Cureality | Real People Seeking Real Cures

I'm itching to say that face-to-face to anyone from the wheat industry--agribusiness, baking, retail distribution . . . anybody. Because it's obvious; it's written on the face . . . and belly, and brain, and knees, and hips. And I believe I will soon have the opportunity.

Taking such a controversial stand in my new book, Wheat Belly, i.e., that wheat products, whole or refined, have NO ROLE IN THE HUMAN DIET whatsoever, was bound to provoke criticism and counterattacks. The wheat world has already taken a blow to the chin with the growing popularity of the (misguided) gluten-free movement and they're going to have to get into the business of media damage control.

Take a look at this press release from the Grain Foods Foundation:

RIDGWAY, COLO. — The Grain Foods Foundation has unveiled plans to counter media publicity attracted by “Wheat Belly.”

“Mullen, working with key members of the Grain Foods Foundation’s scientific advisory board, is addressing ‘Wheat Belly’ through proactive media outreach and its ongoing rapid response program,” said Ashley Reynolds, a Mullen account executive. “In particular, the public relations team will be contacting health and nutrition reporters at print and on-line media outlets, as well as editors at major women’s magazines to influence any diet-related stories that may be published in the coming months.”

. . . Ms. Reynolds, a registered dietitian, noted the author relies on anecdotal observations rather than scientific studies; wheat elimination “means missing out on a wealth of essential nutrients;” six servings of grain-based foods are recommended daily in the Dietary Guidelines for Americans; healthy weight loss depends on energy balance rather than elimination of specific foods; and elimination of wheat products makes sense only for those with medical diagnoses such as celiac disease or gluten sensitivity.

She said the group will lean on its scientific advisory board members to “discredit the book and ensure our messages are backed by sound science. “

Here's some of their starting salvos on their Six Servings Blog.

This reminds me of the fight with Big Tobacco in the '70s: "No, sir, we in the tobacco industry know of no research demonstrating that smoking is bad for health," complete with shots of tobacco executives puffing away on cigarettes.

So brace yourself for a fight. These people are protecting a multi-billion dollar franchise, not to mention their livelihoods and incomes. It could get ugly.

Wheat Belly is finally available in Barnes and Noble and all major bookstores nationwide! Also available at Amazon. Electronic versions for Nook and Kindle, as well as an audio CD, will also be available.

The notion of Wheat Belly got its start right here on The Heart Scan Blog and the diet developed for the Track Your Plaque program to conquer heart disease and plaque.

Chapters in the book include:

Not Your Grandma's Muffins: The Creation of Modern Wheat
Whence and where did this familiar grain, 4 1/2-foot tall "amber waves of grain," become transformed into a 2-foot tall, high-yield genetically unique plant unfamiliar to humans? And why is this such a bad thing?

Cataracts, Wrinkles, and Dowager's Humps: Wheat and the Aging Process
If you thought that bagels and crackers are just about carbs, think again. Wheat consumption makes you age faster: cataracts, crow's feet, arthritis . . . you name it, wheat's been there, done that and brings you one step closer to the big nursing home in the sky with every bite.

My Particles are Bigger than Your Particles
Why consuming plenty of "healthy whole grains" is the path to heart disease and heart attack and why saying goodbye to them is among the most powerful strategies around for reduction or elimination of risk.

Hello, Intestine: It's Me, Wheat
No discussion of wheat is complete without talking about how celiac disease and other common intestinal ailments, like acid reflux and irritable bowel syndrome, fit into the broader concept of wheat elimination.

Here's a YouTube video introduction to the book and concept posted on the YouTube Wheat Belly Channel. Also, join the discussions on The Wheat Belly Blog and Facebook. Have that last bite of blueberry muffin, because I predict you won't be turning back!

No, this is not a discussion of monounsaturated versus hydroxgenated fat. This is about the relatively benign fat that accumulates on your hips, rear end, or arms--the "good"--versus the deep visceral fat that encircles your intestines, kidneys, liver, pancreas, and heart--the "bad."

And I'm not talking about what looks good or bad. We've all seen the unsightly flabby upper arms of an overweight woman or the cellulite on her bulging thighs. It might look awful but, metabolically speaking, it is benign.

It's that muffin top, love handle, or wheat belly that encircles the waist, a marker for underlying deep visceral fat, that:

--Increases release of inflammatory mediators/markers like tumor necrosis factor, leptin, interleukins, and c-reactive protein
--Is itself inflamed. When examined under a microscope, visceral fat is riddled with inflammatory white blood cells.
--Stops producing the protective hormone, adiponectin.
--Traffics in fatty acids that enter the bloodstream, resulting in greater resistance to insulin, fat deposition in the liver (fatty liver), and increases blood levels of triglycerides
--Predicts greater cardiovascular risk. A flood of recent studies (here's one) has demonstrated that larger quantities of pericardial fat (i.e., visceral fat encircling the heart, visible on a CT scan or echocardiogram) are associated with increased likelihood of coronary disease and cardiovascular risk.

You can even have excessive quantities of bad visceral fat without much in the way of fat elsewhere. You know the body shape: skinny face, skinny arms, skinny legs . . . protuberant, flaccid belly, the so-called "skinny obese" person.

Nobody knows why fat in visceral stores is so much more evil and disease-related than, say, wheat on your backside. While you may struggle to pull your spreading backside into your jeans, it's waist girth that is the problem. You need to lose it.

You could take vitamin D and achieve a desirable blood level of 25-hydroxy vitamin D (I aim for 60-70 ng/ml), or you could:

--Take Actos to mimic the enhanced insulin sensitivity generated by vitamin D
--Take lisinopril to mimic the angiotensin-converting enzyme blocking, antihypertensive effect of vitamin D
--Take Fosamax or Boniva to mimic the bone density-increasing effect of vitamin D
--Take Celexa or other SSRI antidepressants to mimic the mood-elevating and winter "blues"-relieving effect of vitamin D
---Take Niaspan to mimic the HDL-increasing, small LDL-reducing effect of vitamin D
--Take naproxen to mimic the pain-relieving effect of vitamin D

So, given a choice, what do most doctors choose? Of course, they choose from the menu as presented by the sexy sales representative sitting in the office waiting room. These medications, of course, are among the top sellers in the drug world, taken by millions of Americans and not just one at a time, but several per person.

The Food and Nutrition Board of the Institute of Medicine, the panel of volunteers charged with drafting a Recommended Daily Allowance for vitamin D, says that you are already getting enough vitamin D, so don't bother taking any supplements and continue to wear your sunscreen. Wonder whose side they're on?

I continue to be impressed that many of the conditions that plague modern people are little more than deficiencies peculiar to modern life, such as vitamin D deficiency, or the result of the excesses of modern life, such as consumption of sucrose, fructose, corn, and "healthy whole grains."

I take 8000 units of gelcap vitamin D and haven't felt better.

A few posts back, I talked about how more people are showing us zero lipoprotein(a) and zero small LDL. That was about 4 weeks ago. By then, I had seen 3 people with zero values on both.

Well, it's now up to 9 people: 9 people who have achieved zero lipoprotein(a) and zero small LDL. These are people who started with typical lipoprotein(a) values of 150-300 nmol/L and small LDL values of 1000-2000 nmol/L, both substantial.

I still don't know how many people or what percentage can expect to show such extravagant results. But the sharp increase over a relatively brief period of time is extremely encouraging!

Heart Scan Blog reader, Frustrated, posted this comment:

Dr. Davis,
I have spent the last 5 months eating a diet that completely eliminated all wheat products. It was very low carb, and consisted of relatively high protein (eggs, grass fed beef, grass fed raw cheese, oily fish, chicken), good level of olive oil, walnuts, fish oil (3 mg per day), raw vegetables, little bit of fruit. So I had good amount of monounsaturated fat as well as saturated fat from eggs and grass fed products.

My recent NMR showed:
LDL-p. 2,800
Small LDL particle 1700
Small HDL particle 20
HDL-C 40
LDL-C 114
Trigs. 224
Total chol 208

So I was disappointed. Where have I gone wrong? No wheat and sky-high LDL-p and 1700 small LDL particles.

This is indeed unusual. I see this perhaps 5 or 6 times over a year's time, while thousands of other people show the usual expected respone. I don't have Frustrated's lipoprotein panel prior to starting the diet, but I'll bet the starting panel was similar to this "after" panel.

The overwhelming majority of people who follow a diet like the one described--no wheat, limited carbohydrate, grass fed beef, fish, chicken, vegetables, limited fruit--obtain extravagant reductions in small LDL, increased HDL, and reduced triglycerides. So why did Frustrated end up with such disappointing results, values that potentially provide for high risk for heart disease?

There are several possibilities:

1) He/she is in the midst of substantial weight loss. When labs are drawn in the midst of weight loss, stored energy is being mobilized into the blood stream. This energy is mobilized as fatty acids and triglycerides which, upon entering the blood stream, cause increased triglycerides, reduced HDL, chaotic or unpredictable small LDL patterns, and increased blood sugar sufficient to be in the diabetic or pre-diabetic range. This all subsides and settles down to better values around 2 months after weight loss has plateaued.

2) Apo E4--If Frustrated has one or two apo E4 genes, then increased dietary fat will serve to exaggerate measures like small LDL despite the reduction in carbohydrates, LDL particle number, and triglycerides. This is a tough situation, since small LDL particles and high triglycerides signal carbohydrate sensitivity, while apo E4 makes this person, in effect, unable to deal with fats and dietary cholesterol. It gives me the creeps to talk about reducing fat intake, but this becomes necessary along with carbohydrate restriction, else statin drugs will come to the "rescue."

3) Apo E2 + Apo E4--It's possible that an apo E2 is present along with apo E4. Apo E2 makes this person extremely carbohydrate-sensitive and diabetes-prone with awful postprandial (after-meal) persistence of dietary byproducts, alongside the hyperabsorption of fats and dietary cholesterol from apo E4. This is a genuine nutritional rock and a hard place.

4) Other variants--There are probably a dozen or more other genetic variants, thankfully rare, such as apo B and apo C2 variants, that are not generally available for us to measure that could influence Frustrated's response.

5) The low-carb diet is not truly low-carb--Frustrated sounds like a pretty sharp cookie. But it's not uncommon for someone to overlook a substantial source of carbohydrate exposure that triggers these patterns. Fruit is a very common tripping point, since people generally regard unlimited fruit as a healthy thing. This does not seem to be Frustrated's problem. Others indulge in quinoa, sweet potatoes, millet or other carbohydrate sources that look and sound healthy but, in sufficient quantities, can still trigger this pattern.

6) Other--Hypothyroidism, kidney disease, nephrotic syndrome, hypercortisolism and some other relatively rare conditions are worth considering if none of the above apply.

Anyway, that's the list I use when this peculiar situation arises. If obvious weight loss is not the culprit, the next step is apo E testing. However, the wrong response is to reject the low-carbohydrate notion altogether and just limit fat, since this typically leads to uncontrolled small LDL, high triglycerides, and diabetes. It can often mean limiting carbohydrates while also limiting fats. Just as with the combination of apo E4 with Lipoprotein(a), I lump many of these patterns into the emerging world of genetic incompatibilities, genetic traits that code for incompatible metabolic phenomena.

A Heart Scan Blog reader posted the link to this very excellent presentation by Dr. David Diamond, a neuroscientist at the University of South Florida.

ATP-3, or Adult Treatment Panel-3, is the set of cholesterol treatment guidelines as established by the National Cholesterol Education Panel, the guidelines used by practicing physicians nationwide. They are also the metric by which the "quality" of care is being judged by agencies like Medicare, health insurers, and other parties interested in policing healthcare. Dr. Diamond ably recounts how we ended up in this mess, the conflagration of "cut your fat, reduce cholesterol, and take a statin drug."

I was very impressed that, in his closing comments, he briefly discusses the pivotal role of glycation in heart disease causation. You will see in coming conversations how important an understanding of glycation is to create a healthy diet and lifestyle.

Conventional thinking is that high LDL cholesterol causes heart disease. In this line of thinking, reducing cholesterol by cutting fat and taking statin drugs thereby reduces or eliminates risk for heart disease.

Here's an (extreme) example of just how far wrong this simpleminded way of thinking can take you. At age 63, Michael had been told for the last 20 years that he was in great health, including "perfect" cholesterol values of LDL 73 mg/dl, HDL 61 mg/dl, triglycerides 102 mg/dl, total cholesterol 144 mg/dl. "Your [total] cholesterol is way below 200. You're in great shape!" his doctor told him.

Being skeptical because of the heart disease in his family, had a CT heart scan. His coronary calcium score: 4390. Needless to say, this is high . . . extremely high.

Extremely high coronary calcium scores like this carry high likelihood of death and heart attack, as high as 15-20% per year. So Michael was on borrowed time. It was damn lucky he hadn't yet experienced any cardiovascular events.

That's when Michael found our Track Your Plaque program that showed him how to 1) identify the causes of the extensive coronary atherosclerosis signified by his high calcium score, then 2) correct the causes.

The solutions, Michael learned, are relatively simple:

--Omega-3 fatty acid supplementation at a dose sufficient to yield substantial reductions in heart attack.
--"Normalization" of vitamin D blood levels (We aim for a 25-hydroxy vitamin D level of 60-70 ng/ml)
--Iodine supplementation and thyroid normalization
--A diet in which all wheat products are eliminated--whole wheat, white, it makes no difference--followed by carbohydrate restriction.
--Identification and correction of all hidden causes of coronary plaque such as small LDL particles and lipoprotein(a)

Yes, indeed: The information and online tools for health can handily exceed the limited "wisdom" dispensed by John Q. Primary Care doctor.

Our new recipes, such as New York Style Cheesecake and Chocolate Coconut Bread, are wheat-free and low- or no-carbohydrate. They fit perfectly into the New Track Your Plaque Diet for gaining control over coronary atherosclerotic plaque, not to mention diabetes, pre-diabetes, hypertension, small LDL particles, high triglycerides, high inflammation (c-reactive protein) and other distortions of metabolism.

However, there's one compromise: We include use of non-nutritive sweeteners. It's therefore important to know that artificial sweeteners are not all created equal.

One common tripping point: maltodextrin.

Maltodextrin is composed of polymers (repeating subunits) of glucose, as few as 3 or as many as 20 or more glucose subunits. So maltodextrin is glucose sugar. While it lacks the especially destructive pentose sugar, fructose, maltodextrin is metabolized to glucose and thereby increases blood sugar substantially.

Many artificial sweeteners are bulked up with maltodextrin. For instance, granulated Splenda and Stevia in the Raw, two sweeteners billed as low-calorie and sugar-free that is used on a cup-for-cup basis like sugar, are primarily maltodextrin--with only a teensy bit of Splenda or stevia.

The best artificial sweeteners, i.e., the most benign without a load of maltodextrin, are:

Liquid stevia--Just the extract from stevia leaves and water. It can be a bit pricey, e.g., $10 for a 2 oz bottle, but a little goes a long way.

Truvia--While I'm not too fond of the manufacturer (Cargill), I believe that Truvia is among the better sweeteners around. It is a mixture of the natural sugar, erythritol, that generates little to no blood sugar effects and rebiana (rebaudioside), an isolate of stevia. Some people aren't too fond of the mild menthol-like cooling effect of the erythritol nor the slight aftertaste. I find it works pretty well in most recipes.

Be aware that, no matter which artificial sweetener you use, it has the potential to stimulate appetite. I therefore like to not eat foods sweetened with liquid stevia or Truvia in isolation but as part of a meal. That way, any appetite stimulation that results is substantially quelled by the proteins and fats ingested.

Former Men's Health editor, Jeff O'Connell, has just released his new book, Sugar Nation.

Back in 2009, Jeff contacted me to obtain some background insights into diabetes and its relationship with diet. He recently sent me a copy of his new book that contains some brief quotes from me.

Jeff is a writer, not a physician nor scientist. But I think that you will find his grasp of diabetes and the nutritional and lifestyle events that led him there far exceed the insights held by most practicing physicians. Like many of us, Jeff discovered how to find his way back from pre-diabetes through lessons he had to learn on his own, but not from his doctor.

Jeff tells this story as reporter, son of an estranged diabetic father with whom he reconnects as he approaches the end of his life, and as fellow sufferer of the pre-diabetic/diabetic mess that modern habits and "official" dietary advice have given us. Jeff's book is worth a read to see yet another dimension of the human stories that are emerging from this incredible nutritional tangle we find ourselves in.

Here's a unique YouTube video about Jeff's story.

Jenny provided permission to reprint her very excellent introduction to low-carbohydrate eating for people with diabetes. You can also view the original version on her Diabetes 101 website.

Jenny is a stickler for monitoring the effects of blood sugar. We might take some lessons from her experiences for improving management of people with metabolic syndrome or borderline blood sugars. In other words, monitoring the blood sugar-raising effects of various foods and food portions can provide great feedback on what foods are preferable, what undesirable, given your physiology.

Even if you are not a diabetic, Jenny's discussion is must reading to gain a better understanding of food choices, particularly carbohydrates. Along with seizing control of health, she has also gained deep wisdom in how to best manage this disease and its physiology.

Introduction to low-carb nutrition for diabetics

It's carbohydrates that raise blood sugar.

Sugars and starches, not the fats that dietitians have been warning you about for so long. If you've been testing your blood sugar after meals, you've probably noticed that already and you are starting to understand why a healthy diabetes diet will have to be one that limits carbohydrates to an amount that doesn't push your blood sugar up over the level where you are damaging your body.

But if your previous experience with restricting carbohydrates involved doing a weight loss diet like Atkins or Protein Power, which worked well for you until you crashed off it entirely and gained back all the weight you'd lost, you may be hesitant to embark on another course of dieting that requires some carb restriction.

I've been there myself. I've done the extremely low carb diet Dr. Richard Bernstein recommends for months on end. I did Protein Power for 3 years. And I've gone on the "Eat all the carbs you didn't eat over the past three years all at once" diet, too. The following observations grew out of my 8 years of experience with learning how to make carb restriction work long-term.

Unlike much of what you've read before, there are no scholarly references for this section. It's based entirely on my own observations and the experience of many dozens of people who have participated in online discussion groups devoted to low carb dieting and diabetes.

Weight Loss Diets Usually Fail but Diabetes Diets Can't Afford To Fail

People who adopt a low carb diet to lose weight tend to start out with great enthusiasm, adapt extreme dieting strategies, swear they will never eat another piece of bread or french fry for the rest of their lives, lose some weight, stall out, burn out, and slink back to their old diets, where they gain back all the weight they lost and more.

This is not a surprise. People on any diet, including low calorie and low fat, do the same thing. The body is very resistant to weight loss and deeply buried instincts in our brains do everything they can to maintain our weights, no matter how unhealthy they might be.

But while this pattern of dieting may be tolerable for those who are dieting to shed a few pounds before their class reunion, it spells disaster for those who must change their diet in order to prevent the high blood sugars that result in amputation, blindness, kidney failure and heart attack death.

Low carbing for diabetes means low carbing for life, long after the thrill has worn off of eating that runny brie and steak. Despite the hype in the diet books, it is not easy, simple, and fun. I know only a handful of people who have been able to sustain a low carb lifestyle for more than five years. And that is after years of online participation in low carb groups.

What you'll find below is what I've found works for me. I used a low carb diet to control my blood sugar for more than five years and have gone through the whole cycle, from enthusiasm, to boredom, to burnout, to saying "To hell with it, we've all got to die some time!" to starting all over again determined to avoid the mistakes that sent me round the bend the first time.

How Many Grams of Carbs to Eat? As Many as Allow You to Reach Your Blood Sugar Targets

When people think about adopting a lower carb diet, their first question is almost always, "How many grams of carbs can I eat at each meal?" Most of the diet books will answer that question with a hard and fast number. Atkins, for example, tells you to start out with 20 grams a day. Protein Power starts you at 30 grams. And Dr. Bernstein suggests 6 grams for breakfast and snacks and 12 grams at lunch and dinner.

Adopting these very low carbohydrate limits will control your blood sugar very nicely. But over time, many people find that sticking to a diet this low in carbohydrate becomes impossible. That's why I'm going to ask you to throw away all those diet books and try a new approach to restricting carbs.

What you will do is to try the strategy used by the people from the alt.support-diabetes newsgroup who informally call themselves "The 5% Club" because their A1c test results fall in the 5% range which doctors consider normal: use your blood sugar meter after each meal to determine how many grams of carbs you can eat and still meet a healthy blood sugar target.

You will start out by measuring your blood sugar one and two hours after each meal. Write down what you ate and observe what it did to your blood sugar. If a meal allows you to reach your blood sugar targets, try eating it again on a different day and test it test again, possibly at a later time, to make sure that your good numbers weren't just a result of slow digestion.

If you end up too high after a meal, the next time you eat it, cut back on the portion size of the carbohydrate elements in the meal and test again. Do this until you can hit your targets, or flag the carbohydrate-containing foods in that meal as ones your body can't handle.

What you're doing here is creating what newsgroup activist Alan S. calls, "a low spike diet" rather than a low carb diet. He can achieve normal post meal blood sugars by eating as many as 30 or 40 grams of carbohydrates at a meal. Others will find that they need to eat a lot less than that amount to hit safe post-meal blood sugar targets.

Usually how much carbohydrate you can manage has something to do with your body size. The more you weigh, the less each gram of carbohydrate you eat will raise your blood sugar. Those of us whose weight is less than 150 lbs often find that we can eat between 12 and 20 grams of carbohydrate and still reach normal blood sugar targets without the help of medications, and that we can add perhaps another 10 or 20 grams more, with medications. People who are much heavier can often eat 30 or 40 grams per meal and still reach their blood sugar targets. In general, men can eat more carbohydrates and still reach their targets than can women, again, because of their larger body size.

How to Learn How Much Carbohydrate is in Your Food

To make this system work, it helps if you start to learn how many grams of carbohydrate are in the foods you eat. That way you won't have to test hundreds of foods once you've learned how a representative sample affect you.

The best way to learn how many grams of carbohydrates are in the different foods you eat is to read food labels carefully, invest in a nutritional guide like one of Connie Netzer's books of nutritional information, download nutrition software like LifeForm (http://www.lifeform.com) or use online calculators like Fit Day (http://www.fitday.com). Software and online sites will compute the amount of carbohydrates and other nutrients in your meal for you as long as you know the portion size.

Learn about Portion Sizes!
This brings up an important point: When you estimate how many grams of carbohydrate there are in a portion of food, it is very important to find out if the amount of food on your plate corresponds to the amount in the "one serving" listed on a label, in a book, or in your software.

The best way to do this is to invest in an electronic food scale and to weigh your foods for a few weeks until you get the hang of estimating portion size. You can get a good food scale at a gourmet kitchen shop for $25 to $40 dollars. This food scale may be the best nutritional investment you'll ever make.

Once you start using your scale, you will find that the muffin you bought at the coffee shop weighs 8 ounces, which is fully four times the 2 ounces that most food databases give as "one serving" of a muffin. When you read that a mythical 2 ounce portion of muffin contains 27 grams of carbohydrate you will realize why that 8 ounce coffee shop muffin with its 108 grams of carbohydrates sends your blood sugar into the psycho zone!

With ice cream, when you weigh your ice cream on a food scale, you'll quickly see that the "one portion" listed on the package turns out to be only a few teaspoons' worth. That bowl you've been considering as one portion of ice cream weighs in as four servings or 72 grams of carbohydrate and 600 calories, which may explain its damaging effect on both your blood sugar and your waistline.

This may sound like a lot of work, and when you first start, it is. But after you do it for a few weeks you'll find you have memorized the carbohydrate gram counts and the portion sizes for the foods you usually eat, and once you have tested your blood after eating these portion sizes, you won't have to test every time you eat a favorite meal, because you will know what it is going to do to your blood sugar.

Eating Away from Home

The biggest challenge you'll encounter as you start learning what you can eat will be eating away from home. You aren't going to be able to weigh restaurant foods nor can you look up the nutritional values of many restaurant offerings--though many of the common fast food outlets do provide nutritional information online--though often without listing portion sizes.

That makes it a very good idea to avoid starchy or sugary restaurant foods or, if you do eat them, to eat only a small portion of what you are offered. Measure your blood sugar an hour or two hours after eating if you aren't sure about how a restaurant food will affect you.

Fat and Carbs Eaten Together will Digest Slowly

Foods with a lot of fat in them take longer to digest than those without a lot of fat. This is why pizza and ice cream often give deceptively good readings on your meter. If you test a meal and see a reading that is too good to be true, be sure you test at 3 or four hours after eating.

The Truth About Pasta

Pasta was long recommended to people with diabetes as a food that would not raise blood sugar and you will still see it starring in many cookbooks and magazines intended for people with diabetes.

However, if you test pasta 4 or 5 hours after eating, you may get an unpleasant surprise. This is true with the so-called "low carb" pastas, too. These foods give you excellent readings at one and two hours because they are resistant to digestion so they don't turn into glucose right away. But five hours later, they do break down into glucose and when they do, the 52 grams of carbohydrates found in each 2 ounce serving of pasta will hit your blood stream with a nasty wallop. (Not to mention that you almost need a microscope to see a 2 ounce portion of pasta. Most people's idea of a portion of pasta is closer to 6 ounces--and 156 grams of carbohydrate!)

If you have pasta for dinner and don't see a peak 3 hours later, be sure to check your fasting blood sugar the next morning. You may see the blood sugar rise there, too.

Sugar Alcohol and "Sugar Free" Foods

The sugar alcohol used in so-called "sugar free" foods can also show up in your blood sugar an hour or two after you'd expect to see them, especially the maltitol used in "sugar-free" candy. At least half of the sugar in Maltitol does turn into glucose in your blood stream and it can raise your blood sugar, but the rise is delayed so you may miss it on testing. So if a "sugar free" food seems to be kind to your blood sugar, try testing it an hour or two after your first tests. Erythritol is the one sugar alcohol that usually does not show up in your blood sugar.

Dealing with Limited Blood Testing Supplies

In in ideal world, we'd all have all the testing supplies we needed to control our blood sugar, but in real life blood sugar test strips are very expensive and many insurers sharply limit the number of strips people with Type 2 diabetes can get each month.

Here are some strategies that can help you if your access to strips is limited.

If you only have 50 strips to get you through a month, plan out what you are going to test ahead of time. Pick one of your favorite meals, and test at 1 hour after eating the first time you eat it and 2 hours after eating the second. Do this with a couple different meals and see if there's a pattern as to when you see the highest reading--whether it is at one hour or two. Then choose another meal and test it at the time when you saw the highest reading in the earlier meal. If you ever get a surprisingly low reading, try testing an hour later or earlier, to make sure you aren't missing the peak.

Make the goal of your testing be learning how many grams of carbs you can tolerate in one meal. If you learn that 30 grams is your upper limit, use software and your scale to find portions of other foods that will also clock in at 30 grams or less. Test one or two of these, and if you see the result you expect, you don't have to test every time you eat these foods again.

Wal-mart sells a cheap and effective blood sugar meter with strips that cost one half as much as other vendors. Some drug stores also sell store brand meters with cheaper strips. If you need more strips, consider the $50 you pay for another 100 strips an investment in your health. It's far better to spend that $50 now, than to spend it on expensive doctor bills caused by complications you don't need to develop!

Keep the focus on Achieving your Blood Sugar Goals

By testing after meals, you'll learn how many grams of carbohydrate your own, unique, body can handle. And more importantly, you'll also be able to decide if you are going to be able to control through diet alone, of whether it is time to talk to your doctor about supplementing dietary control with drugs.

Many people are so excited to learn that they can achieve normal blood sugars by cutting way back on carbohydrates that they become zealots for low carb dieting. I've been there and I've done that. But it's important not to get too carried away with a "Carbs are Evil" mentality which makes it a matter of religious zeal never to let evil carbs cross your lips again. Like all conversions this one tends to fade out in time. And as we said at the start of this chapter, your ultimate goal is to maintain your blood sugar targets for the rest of your life. So the safest approach is to get the most blood sugar benefit you can out of restricting carbohydrates, but restrict them to a level you can maintain year in and year out.

Most importantly, I have learned it is best to treat carb restriction as a strategy, one of many, which used in combination with other strategies including medications if needed, can give you normal blood sugars, rather than the One and Only True Way. If you can be flexible and find more than one tool to help you meet your blood sugar targets, you are more likely to be able to maintain those excellent blood sugars for years to come.

Eliminate "Habit Carbs" and Concentrate on "Value Carbs"
When people think about restricting their carb intake they assume this means never eating any of their favorite foods again.

But for many of us, this doesn't have to be true. Why? Because a quick look at your daily carb intake will often reveal that the bulk of the carbohydrates you are eating are what I call "habit carbs." These are the carbs you eat without a second thought because they are there. Not because they taste good. Not because you couldn't live without them. Just because you're in the habit of eating them.

Here is a list of some prime "habit carbs."

Steam table mashed potatoes

Limp french fries

Squashy hamburger buns

Cardboard toast

Cold home fries

Stale boxed cookies

How many of these flavorless, starchy foods are you consuming everyday just because they're there? Probably more than you realize. So before you lift that fork-full to your mouth, ask yourself, "Is this food thrilling me?" If not, put it down. This should go a long way towards getting your carb intake down.

What I'd call "value carbs" are those carb-rich foods that really do mean something to you. I'm not going to lie to you. You are not going to be able to make them the mainstays of your diabetes diet. But by using the strategies describe below, you should be able to eat enough of these foods to keep yourself from feeling deprived--without destroying your health.

Don't Create "Forbidden Foods!"

If you are one of those people who could live happily on Purina People Chow, you can skip what follows. But if food has been important to you, and if you have hitherto had a long and emotionally satisfying relationship with food, or if, like me, baking from scratch was one of your favorite ways to show love and express creativity, restricting your carbohydrate input will mean that a whole lot of what you've been eating (and baking) up until now is suddenly, completely, off limits. I can't eat cake and get a healthy blood sugar level. Even with two different diabetes drugs in my system. I can't eat cake even with an insulin shot before I eat it. I love cake but there is no way I can eat more than a bite or two without seeing very high blood sugars and there is no way I can eat two bites of cake and be happy. The same goes for french fries and Thai noodles.

During the first enthusiastic weeks of exploring carb restriction most people deal with this kind of discovery by coming up with new recipes and finding new, delicious and healthy things they can substitute for old, high carb standards. They appreciate the way cutting way back on carbohydrates curbs their hunger and makes food much more manageable. This is good and it is why long term low carbing is possible. But our old favorite foods do not go away that easily.

If you decide that some food you have been eating and enjoying all your life will never again cross your lips, it is almost 100% guaranteed that you'll end up pigging out on that very same food at some time in the future, hating yourself, and even beginning a binge that can throw you completely off your diet for months.

It might not happen the first month you are restricting your carb intake or even the first year. It took me three years of low carbing to get to where I crashed off my stringent low carb diet. But eventually it happens, and because after almost a decade of counting my carbs I've learned that I will never lose my love for certain foods that don't love me, I've put a lot of time into finding a way of restricting my carbohydrate intake in a way that avoids the buildup those feelings of deprivation that eventually lead to long periods of unwise eating.

The key, for me, is to build safety valves into my diet. I don't call them "cheats" or "bad foods" for reasons I'll get into later. I call them "off plan" foods because they are not food I can make an ongoing part of my daily food plan. Because my goal is life-long blood sugar control, I accept that I will occasional eat "off plan" and that this is okay as long as I am meeting my blood sugar targets most of the time. "Good enough" control that I can adhere to year in and year out beats a few months of perfection followed by crashing off the diet entirely and ruining my health. Here is one way to approach doing this:

Do the Diet Straight for a Month or Two Before You Try Off-Plan Goodies

As you learn what foods raise your blood sugar and what foods don't, you will almost certainly find that there are a lot of foods you used to love that don't work for you anymore. Waffles for breakfast, coffee cake at coffee break, three slices of pizza with crust, a burger with a bun and a side of fries are just a few of the foods that it is almost certain will not allow you to meet your post-meal blood sugar targets.

As you keep using your meter to test what you eat, if you are like most people with diabetes you'll also learn that some of the so-called "low glycemic" foods and the supposedly "healthy" whole grains that nutritionists recommend for people with diabetes won't work either. Oatmeal and whole wheat bagels raise my blood sugar far too high, so does cracked whole wheat, whole wheat bread, and brown rice.

If the dietician tells you a food is good for you, but your meter tells you it is raising your blood sugar to a level that is high enough to cause complications, you will have to listen to your meter. Your meter will tell you what is safe to eat and for the first couple of months while you are learning how to get your blood sugar under control and how bring those high blood sugars down to normal levels you will have to accept that you can only eat those foods that don't cause spikes.

If you attempt to add in off-plan foods before you are solidly on-plan you may never really get into the swing of eating a diet that controls your blood sugars and you may not get to where your body learns to enjoy the lower carb foods that don't give you blood sugar swings.

But after you've gotten your blood sugar under control, nothing horrible will happen if you make room for a small portion of some high carb treat every now and then.

How to Add Off-Plan Foods to the Plan

If you've avoided bread for a couple months, the humble roll in that restaurant bread basket may start to call out to you with an irresistible siren song. If you give in and eat it, with each bite you may find yourself feeling as if you are doing something incredibly sinful--the way you might have felt if you had eaten a whole box of chocolates in the past.

That feeling is the sign that you're heading for trouble. You've created a "forbidden fruit" and sooner or later that forbidden fruit is going to get you. You may find yourself thinking about that roll, craving another, sneaking off to eat one where nobody knows you, or, alternatively, you may declare that you will never again eat a roll ever--and then ruin your Thanksgiving holiday when you go to Aunt Glenda's and refuse to eat even a single one of those wonderful rolls of hers you've eaten every year of your life which say, "This is the family Thanksgiving" to you.

It is far better to make a bit of room in your diet for high carb treats so that they don't build up a charge. If you do this, you'll find that they almost never taste as good as you remembered, and you'll be able to leave them behind without turning them into an object of obsession.

Just knowing that you can eat some specific off-plan food at some future time, when it is scheduled, makes it that much easier to say, "No thanks" to it, and maintain your healthy blood sugar the rest of the time.

How Often Can You Eat Off-Plan?
How often you have an off-plan food depends a lot on your dietary goals, how high your blood sugar is before you eat carbs, and whether you are willing to exercise after eating. It also depends greatly on what medications you are taking for your diabetes. Whatever I eat, I try to keep my blood sugar below 120 mg/dl (6.7 mmol/l) at 2 hours after any meal.

Forty minutes of cardiovascular exercise will burn off a lot of extra carbs, so if you exercise regularly, try to eat your high carb treat before you head for the gym.

If you're trying to lose weight, you may have to keep off plan treats few and far between. When I was actively losing weight on a low carb diet without medications I ate one off-plan meal about once every two weeks.

Once I reached my weight loss goal I loosened up a bit but I found it best to cycle between weeks of eating a strict very low carb diet, and then a week of eating slightly more carbs--but I tried very hard not to ever anything that would cause my blood sugar to be over 120 mg/dl (6.7 mmol/L) at 2 hours after a meal because doing so makes me feel rotten.

Throw Away the Vocabulary of Self-Destructive Dieting

When you eat something with carbs in it, don't think of it as a "cheat." Cheating is what you do when faced with an authority figure--your 9th grade math teacher or the IRS. But you are the one in control of what you eat. So when you eat something that is off-plan, you should stop thinking of it as "getting away with something" and treat it instead as something you've decided to do--for a reason that should be clear to you while you do it.

If you keep eating things that were not what you had intended, rather than beating yourself up, it's time to reconsider your food plan and figure out why it isn't working. Are you having trouble finding foods in restaurants that don't raise your blood sugar? Maybe it's time to bring your lunch along to work for a while, or to find new place to dine.

Are you bored with what you have been eating? Google for good low carb recipes you can try at home. There are thousands of them. If you use the Google Groups search and look for messages in alt.support.diet.low-carb that start with "REC" you'll find a treasure trove of ideas to try.

Keep the vocabulary of sin and guilt for the confessional. You're going to eat a lot of things in the years to come that will mess up your blood sugar. But if you are kind to yourself and dust yourself off after you mess up and keep on going, doing the best you can to hit your blood sugar targets, you may very well end up healthier than many people who do not have diabetes. The important thing is to keep at it, doing the best you can and forgiving yourself when the best you can do isn't as good as you wish it was.

Know Your Limits
I've learned the hard way I can't eat half a blueberry muffin, so I don't even try portion control for that particular food. I know blueberry muffins are trouble and I also know that I will eventually eat one. That's just how it is, so every blue moon or so I eat a blueberry muffin, experience the miserable high blood sugars that follow, and then remember why I don't eat muffins every day any more. What I don't do is fool myself that I can buy a muffin and only eat half. Everyone has a few foods that fall into this category. Treat them with caution!

Eat Off-Plan Foods Out of the House
I've learned the hard way that if a big box of something full of carbs is in the fridge, bad things are going to happen. So I try to eat my off-plan foods away from home. I eat my muffins or cookies at a coffee house. I have a slice of pizza at a pizzeria. I don't buy a box of muffins or a whole pizza and bring them home.

Getting this strategy to work requires that your whole family understand what's at stake. It took me a couple years of harping on what "complications" means, but by now, my family understands that if my blood sugar is too high, I'm damaging my body. They want to keep me around for a while, so they understand that there are some foods that shouldn't be brought into the house--ever.

When other family members want to have treats at home, they are kind enough to buy things I don't like. For example, if someone wants Ben & Jerry's they buy the Chunky Monkey flavor that I find revolting, not the New York Fudge. By the same token, when my kids lived at home, I didn't buy them the brands of cookies I can't resist. There are plenty of others cookies they liked that don't tempt me at all, and those were the ones in the cupboard.

Over the years the nondiabetic members of my family learned that no one is doing themselves a favor scarfing down 300 grams of fast acting carbohydrate every day--particularly not people with a family history of diabetes and heart disease!

Medications Can Help

I'm not a big fan of medications because I've learned the hard way that drug companies lie about side effects and some of these side effects are permanent and can ruin your life. But I learned the hard way, too, that some of us (like, say me) can't get normal blood sugars no matter how low our carb intake. For us, adding a diabetic drug or two to our daily regimen may be the only way we can get normal blood sugars without a life of tormenting self-denial.

Drugs I have found useful over the years include metformin, precose, and post-meal insulin shots. The new incretin drugs, Januvia and Byetta help some people make dramatic improvements in their blood sugar, but the way that they work makes it necessary to eat a slightly higher amount of carbohydrates with them because they only work when your blood sugar rises over a certain threshold. Even with these drugs (including Januvia) I've never been able to eat more than 120 grams of carbohydrates a day, but after many years of eating an extremely low carb diet--which was the only diet that would control my blood sugars--120 grams of carbs a day feels like a completely normal diet!

Be Aware of Rising Insulin Resistance

Some people may find that eating a low carb diet is not enough to control their blood sugar because they are very insulin resistant. Perhaps they have been diagnosed with PCOS, or have to take a drug, like Prednisone that increases insulin resistance. The book, Dr. Bernstein's Diabetes Solution by Dr. Richard K. Bernstein, the distinguished diabetes doctor, recommends Metformin as an appropriate drug for patients on a low carb diet whose blood sugars are still not completely controlled. It isn't a cure by any means, just one more tool you can use to keep blood sugars under control, and if you limit your insulin resistance you may solve both weight and hunger problems that otherwise can derail your diet.

You can read more about the different drugs available to help control blood sugars HERE. Just remember that all these diabetes drugs work best when you combine them with some level of carbohydrate restriction. How much restriction? Test your meals one and two hours after eating, and your blood sugar meter will tell you exactly how much.

Top Medical Journal Publishes Landmark Study Showing Very Low Carb Diet Most Effective and Safest for Lipids etc.

In case you are still being given out-of-date medical or nutritional advice by people who tell you that a low carb/high fat diet will give you a heart attack, take a look at this recently published study, which appeared in the Journal of the American Medical Association.

This study found that an Atkins style low carb diet not only caused double the weight loss of the low fat diet at the end of one year, but it did not adversely affect cholesterol levels.

This finding, added to the Women's Health Initiative finding (after $40 million dollars of research) that low fat dieting does NOT prevent heart disease, should lay to rest any last fears you might have about the impact of cutting carbs on your health.

The findings of this study, are not news to anyone who has tried a low carb diet and stuck with it for any period of time, but they appear to amaze the entire medical community who continue to cling to their to the "Fat is Bad" religious belief long no matter what evidenced-based medical studies might come up with.

Bottom line: You can cut your carbs way down, replace carbs with fat, and await the better health this kind of eating will provide.

Comparison of the Atkins, Zone, Ornish, and LEARN Diets for Change in Weight and Related Risk Factors Among Overweight Premenopausal Women: The A TO Z Weight Loss Study: A Randomized Trial.Christopher D. Gardner, PhD; Alexandre Kiazand, MD; Sofiya Alhassan, PhD; Soowon Kim, PhD; Randall S. Stafford, MD, PhD; Raymond R. Balise, PhD; Helena C. Kraemer, PhD; Abby C. King, PhD

Here's the summary of the WHI findings:

NIH News: News from the Women?s Health Initiative: Reducing Total Fat Intake May Have Small Effect on Risk of Breast Cancer, No Effect on Risk of Colorectal Cancer, Heart Disease, or Stroke

Here's a study that documents the effectiveness of lowering carbs and increasing fat and protein consumption for the control of blood sugar in the absense of weight loss:

Control of blood glucose in type 2 diabetes without weight loss by modification of diet composition. Nutrition & Metabolism 2006, 3:16.

To Get More Help with Making a Low Carbohydrate Diet Work

My "Low Carb Facts and Figures" site, which now shares this server, has more information I collected back in the days when I used a low carb diet for both weight loss and blood sugar control.

You'll find articles there that address a few of the issues people run into while eating a very low carb diet,which are not answered in a completely honest fashion by the people who sell diet books promising you can lose weight easily while gorging on all your favorite foods--which, sadly, is 99% of all authors writing diet books.

In his most recent Vitamin D Council Newsletter (reprinted in its entirety below, minus clickable links, as Dr. Cannell apparently lost his webmaster and this issue of the newsletter is therefore not posted on the Vitamin D Council website; if you would like to either donate money to the Vitamin D Council or pitch in with help with his website, go to www.vitamindcouncil.com), Dr. John Cannell once again enlightens us with some new insights into vitamin D and its enormous role in health. In this issue, he discusses the role of vitamin D in people diagnosed with cancer (treatment, not prevention).

While cancer is not our focus on the Heart Scan Blog, Dr. Cannell's always insightful comments provide some helpful thoughts for our management of vitamin D doses and blood levels.

Dr. Cannell cites a recent study from vitamin D research expert, Dr. Bruce Hollis:

In the first study of its kind, Professor Bruce Hollis of the Medical University of South Carolina gave all of us something to think about. He asked and answered a simple question: How much vitamin D do you have to take to normalize the metabolism of vitamin D?

Remember, unlike other steroid hormones, vitamin D has very unusual metabolism in most modern humans, called first-order, mass action, kinetics. All this means is that the more vitamin D you take, the higher the 25(OH)D level in your blood, and the higher the 25(OH)D level in your blood, the higher the levels of activated vitamin D in your tissues. No other steroid hormone in the body behaves like this. Think about it: would you like your estrogen level to be dependent on how much cholesterol you ate? Or your cortisol level? (I'd ask the same about testosterone levels but I know men well enough not to ask.) No, the body must tightly regulate powerful steroid hormones through substrate inhibition, that is, if an enzyme turns A into B, when the body has enough B, B inhibits the enzyme and so limits its own production.

Not so with vitamin D, at least at modern human vitamin D levels. Professor Reinhold Vieth was the first to write about this and Vieth's Chapter 61 in Feldman, Pike, and Glorieux's wonderful textbook, Vitamin D (Elsevier, 2005, second edition), is a great reason to buy the textbook or have your library do so. (I'm glad to see Amazon is out of stock of the new ones (someone must be reading about vitamin D) but you can still buy used editions.)

Why would the kinetics of vitamin D be different from all other steroids? Maybe they are not, Hollis reasoned, like Vieth before him. Maybe vitamin D levels are so low in modern humans that its metabolic system is on full blast all the time in an attempt to give the body all the vitamin D metabolites it craves. So Hollis asked, Is vitamin D's metabolism different in populations in the upper end of 25(OH)D levels (a population of sun-exposed people and a group of women prescribed 7,000 IU per day)? Note, the Hollis study is free on Medline, you can download the entire paper on the right hand of the PubMed page below.

Hollis BW, et al. Circulating vitamin D3 and 25-hydroxyvitamin D in humans: An important tool to define adequate nutritional vitamin D status. J Steroid Biochem Mol Biol. 2007 Mar;103(3-5):631-634.

If you look at the two graphs, Figures 1 and 2 of Hollis' paper, you find vitamin D's kinetics can be normalized, made just like all other steroid hormones in the body, but you have to get enough sunshine or take enough vitamin D to get your 25(OH)D level above 50 ng/ml, and 60 ng/ml would be better. Then your body starts to store cholecalciferol in the body without much further increase in 25(OH)D levels. The reaction becomes saturable. This is a remarkable discovery and it implies levels of 30 and 40 ng/ml are usually not sufficient. It also implies actual vitamin D levels (cholecalciferol levels), not just 25(OH)D levels, may be useful in diagnosing and treating deficiency. Note, that not all of the sun-exposed individuals or women prescribed 7,000 IU/day achieved such levels. That's because the sun-exposed individuals were tested after an Hawaiian winter and because prescribing and taking are two different things.

In answer to the question, "How much vitamin D should someone with cancer take?," Dr. Cannell advises:
"Take enough to get your 25(OH)D level above 60 ng/ml, summer and winter." In doing so, you will have normalized the kinetics of vitamin D and stored the parent compound, cholecalciferol, in your tissues. In the absence of sunshine, you need to take about 1,000 IU/day per 30 pounds of body weight to do this. A 150 pound cancer patient may need to take 5,000 IU per day, a 210 pound cancer patient about 7,000 IU per day, all this in the absence of sunlight.

Dr. Cannell, no stranger to the resisitance among many practicing physicians unaware of the expanding and robust literature on vitamin D, advises people with cancer that:
In the end, if you have cancer and your physician won't do a risk/benefit analysis, do it yourself. The risk side of that equation is easy. Both Quest Diagnostics and Lab-Corp, the two largest reference labs in the USA, report the upper limit of 25(OH)D normal is 100 ng/ml and toxic is above 150 ng/ml, so 60 ng/ml is well below both. The reason levels up to 100 ng/ml are published normals is because there is no credible evidence in the literature that levels of 100 ng/ml do any harm and because sun worshipers often have such levels. (If you don't believe me, go to the beach in the summer for one month, sunbath every day for 30 minutes on each side in your bathing suit, and go home and have a 25(OH)D level.) By getting your level above 60 ng/ml, all you are doing is getting your levels into the mid to upper range of laboratory reference normals. Little or no risk.

For readers wishing to read the entire text of Dr. Cannell's newsletter, it is reprinted below:

The Vitamin D Newsletter
January, 2008

The January newsletter is coming early as I will be out of touch for awhile. If you remember, the last newsletter was on preventing cancer, not treating it. Below is a sampling of the tragic emails the last newsletter generated:

"Dr. Cannell, I was just diagnosed with breast cancer, how much vitamin D should I take?"

"My mother has colon cancer, how much vitamin D should she take?"

"I've had prostate cancer for four years, is there any reason to think vitamin D would help?"

"Dr. Cannell, my son has leukemia, should I give him vitamin D?"

It's one thing to talk about evidence vitamin D may prevent cancer but something quite different to discuss evidence vitamin D might help treat cancer. I used to think the answers to all the above questions were the same. Like anyone else, people with cancer should be screened for vitamin D deficiency and be treated if deficiency is present. Simple. However, it's not that simple. The real questions are, What are reasonable 25-hydroxy-vitamin D [25(OH)D] levels for someone with a life-threatening cancer? How much vitamin D do they need to take to obtain such levels? Is there any evidence, of any kind, that vitamin D will help treat cancer? The risk/benefit analysis of taking vitamin D is quite different if you are in perfect health than if your life, or your child's life, is on the line.

Remember, unlike cancer prevention, not one human randomized controlled trial exists showing vitamin D has a treatment effect on cancer. By treatment effect, I mean prolongs the lives of cancer patients. However, as I cited in my last newsletter, Dr. Philippe Autier of the International Agency for Research on Cancer, and Dr. Sara Gandini of the European Institute of Oncology, performed a meta-analysis of 14 randomized controlled trials showing even low doses of vitamin D extend life but they looked at all-cause mortality, not just cancer (Arch Intern Med. 2007;167(16):1730-1737). However, some epidemiological studies indirectly address the treatment issue and are quite remarkable. The first are a series of discoveries by Professor Johan Moan, Department of Physics at the University of Oslo, with Dr. Alina Porojnicu as the lead author on most of the papers.

Moan J, et al. Colon cancer: Prognosis for different latitudes, age groups and seasons in Norway. J Photochem Photobiol B. 2007 Sep 19

Lagunova Z, et al. Prostate cancer survival is dependent on season of diagnosis. Prostate. 2007 Sep 1;67(12):1362-70.

Porojnicu AC, et al. Changes in risk of death from breast cancer with season and latitude: sun exposure and breast cancer survival in Norway. Breast Cancer Res Treat. 2007 May;102(3):323-8.

Porojnicu A, et al. Season of diagnosis is a predictor of cancer survival. Sun-induced vitamin D may be involved: a possible role of sun-induced Vitamin D. J Steroid Biochem Mol Biol. 2007 Mar;103(3-5):675-8.

Porojnicu AC, et al. Season of diagnosis is a prognostic factor in Hodgkin's lymphoma: a possible role of sun-induced vitamin D. Br J Cancer. 2005 Sep 5;93(5):571-4.

Porojnicu AC, et al. Seasonal and geographical variations in lung cancer prognosis in Norway. Does Vitamin D from the sun play a role? Lung Cancer. 2007 Mar;55(3):263-70.

What Professor Moan's group discovered, repeatedly, is quite simple, whether it be cancer of the breast, colon, prostate, lung, or a lymphoma. You live longer if your cancer is diagnosed in the summer. And it is not just Moan's group who has found this. A huge English study recently confirmed Moan's discovery.

Lim HS, et al. Cancer survival is dependent on season of diagnosis and sunlight exposure. Int J Cancer. 2006 Oct 1;119(7):1530-6.

What do these studies mean? Something about summer has a treatment effect on cancer. Whatever it is, you live longer if you are diagnosed in the summer but die sooner if you are diagnosed in the winter. What could it be about summer? Exercise? Fresh air? Melatonin? Sunlight? Pretty girls? Remember, these patients already had cancer. Whatever it is about summer, it is not a preventative effect that Professor Moan discovered, it is a treatment effect. Something about summer prolongs the life of cancer patients.

Dr. Ying Zhou, a research fellow, working with Professor David Christiani at the Harvard School of Public Health, went one step further. The stuffy Harvard researchers assumed summer worked its magic, not by pretty girls, but by summer sunlight making vitamin D. So they looked at total vitamin D input, from both sun and diet, to see if high vitamin D input improved the survival of cancer patients. Yes, indeed, remarkably. They found that early stage lung cancer patients with the highest vitamin D input (from summer season and high intake from diet) lived almost three times longer than patients with the lowest input (winter season and low intake from diet). Three times longer is a huge treatment effect, a treatment effect that most conventional cancer treatment methods would die for.

Zhou W, Vitamin D is associated with improved survival in early-stage non-small cell lung cancer patients. Cancer Epidemiol Biomarkers Prev. 2005 Oct;14(10):2303-9.

And that's not all, Marianne Berwick and her colleagues, at the New Mexico Cancer Institute, found malignant melanoma patients with evidence of continued sun exposure had a 60% mortality reduction compared to patients who did not. That implies a robust treatment effect from sunlight.

Berwick M, et al. Sun exposure and mortality from melanoma. J Natl Cancer Inst. 2005 Feb 2;97(3):195-9.

I will not list the thousands of animal studies that indicate vitamin D has a treatment effect on cancer as almost all of them studied activated vitamin D or its analogs, drugs that bypass normal regulatory mechanisms, cannot get autocrine quantities of the hormone into the cell, and that often cause hypercalcemia. However, Michael Holick's group found that simple vitamin D deficiency made cancers grow faster in mice. That is, vitamin D has a cancer treatment effect in vitamin D deficient mice. Professor Gary Schwartz, at Wake Forest, recently reviewed the reasons to think that vitamin D may have a treatment effect in cancer.

Tangpricha V, et al. Vitamin D deficiency enhances the growth of MC-26 colon cancer xenografts in Balb/c mice. J Nutr. 2005 Oct;135(10):2350-4.

Schwartz GG, Skinner HG. Vitamin D status and cancer: new insights. Curr Opin Clin Nutr Metab Care. 2007 Jan;10(1):6-11.

Finally, one human interventional study exists. In 2005, in an open trial, Professor Reinhold Vieth and his colleagues found just 2,000 IU of vitamin D per day had a positive effect on PSA levels in men with prostate cancer.

Woo TC, et al. Pilot study: potential role of vitamin D (Cholecalciferol) in patients with PSA relapse after definitive therapy. Nutr Cancer. 2005;51(1):32-6.

So we come back to the crucial question. If you have cancer, how much vitamin D should you take, or, more precisely, what 25(OH)D level should you maintain? We don't know. You can correctly say that definitive studies have not been done and, incorrectly, conclude physicians treating cancer patients should do nothing. I say incorrectly because standards of medical practice have always demanded that doctors make reasonable decisions based on what is currently known, doing a risk/benefit analysis along the way to decide what is best for their patients based on what is known today. If a patient has a potentially fatal cancer, the doctor cannot dismiss a relatively benign potential treatment modality just because definitive studies have not been done, and passively watch his patient die. Standards of care require doctors consider what is known now, using information currently available, perform a risk/benefit analysis, and then act in the best interest of their patient.

Luckily, such doctors recently obtained some guidance. In the first study of its kind, Professor Bruce Hollis of the Medical University of South Carolina gave all of us something to think about. He asked and answered a simple question: How much vitamin D do you have to take to normalize the metabolism of vitamin D?

Remember, unlike other steroid hormones, vitamin D has very unusual metabolism in most modern humans, called first-order, mass action, kinetics. All this means is that the more vitamin D you take, the higher the 25(OH)D level in your blood, and the higher the 25(OH)D level in your blood, the higher the levels of activated vitamin D in your tissues. No other steroid hormone in the body behaves like this. Think about it, would you like your estrogen level to be dependent on how much cholesterol you ate? Or your cortisol level? (I'd ask the same about testosterone levels but I know men well enough not to ask.) No, the body must tightly regulate powerful steroid hormones through substrate inhibition, that is, if an enzyme turns A into B, when the body has enough B, B inhibits the enzyme and so limits its own production.

Not so with vitamin D, at least at modern human vitamin D levels. Professor Reinhold Vieth was the first to write about this and Vieth's Chapter 61 in Feldman, Pike, and Glorieux's wonderful textbook, Vitamin D (Elsevier, 2005, second edition), is a great reason to buy the textbook or have your library do so. [ I'm glad to see Amazon is out of stock of the new ones (someone must be reading about vitamin D) but you can still buy used editions.)

Why would the kinetics of vitamin D be different from all other steroids? Maybe they are not, Hollis reasoned, like Vieth before him. Maybe vitamin D levels are so low in modern humans that its metabolic system is on full blast all the time in an attempt to give the body all the vitamin D metabolites it craves. So Hollis asked, Is vitamin D's metabolism different in populations in the upper end of 25(OH)D levels (a population of sun-exposed people and a group of women prescribed 7,000 IU per day)? Note, the Hollis study is free on Medline, you can download the entire paper on the right hand of the PubMed page below.

Hollis BW, et al. Circulating vitamin D3 and 25-hydroxyvitamin D in humans: An important tool to define adequate nutritional vitamin D status. J Steroid Biochem Mol Biol. 2007 Mar;103(3-5):631-4.

If you look at the two graphs, Figures 1 and 2 of Hollis' paper, you find vitamin D's kinetics can be normalized, made just like all other steroid hormones in the body, but you have to get enough sunshine or take enough vitamin D to get your 25(OH)D level above 50 ng/ml, and 60 ng/ml would be better. Then your body starts to store cholecalciferol in the body without much further increase in 25(OH)D levels. The reaction becomes saturable. This is a remarkable discovery and it implies levels of 30 and 40 ng/ml are usually not sufficient. It also implies actual vitamin D levels (cholecalciferol levels), not just 25(OH)D levels, may be useful in diagnosing and treating deficiency. Note, that not all of the sun-exposed individuals or women prescribed 7,000 IU/day achieved such levels. That's because the sun-exposed individuals were tested after an Hawaiian winter and because prescribing and taking are two different things.

So my answer to "How much should I take if I have cancer?" is "Take enough to get your 25(OH)D level above 60 ng/ml, summer and winter." In doing so, you will have normalized the kinetics of vitamin D and stored the parent compound, cholecalciferol, in your tissues. In the absence of sunshine, you need to take about 1,000 IU/day per 30 pounds of body weight to do this. A 150 pound cancer patient may need to take 5,000 IU per day, a 210 pound cancer patient about 7,000 IU per day, all this in the absence of sunlight. And this may not be enough; cancer patients may use it up faster (increased metabolic clearance) and children may do the same due to their young and vital enzymes. Or you may need less, because you get more sun than you think, more from your diet, or because you are taking a modern medicine that interferes with the metabolism of vitamin D. An even easier way to do it is go to a sun tanning booth every day and obtain and keep a dark, full-body, tan. Then you don't have to worry about blood levels but I'd get one anyway, just to be sure it was above 60 ng/ml.

Given what Hollis discovered, given the well-known potent anti-cancer properties of activated vitamin D, given epidemiological evidence that summer extends the life of cancer patients, given a meta-analysis of randomized controlled trials showed that vitamin D prolongs life, given animal data that simple vitamin D has a treatment effect on cancer, and given a patient with a life-threatening cancer, what would a reasonable physician do? Simply let their patient die while muttering something about the lack of randomized controlled trials?

No, they would simply check a 25(OH)D level every month and advise cancer patients to take enough vitamin D or frequent sun tanning parlors enough to keep their level above 60 ng/ml. Toxicity does not start until levels reach 150 ng/ml but if you take more than 2,000 IU per day have your doctor order a blood calcium every month or two along with the 25(OH)D. Both you and he will feel better and because if you have cancer, you are probably taking lots of other drugs and little is known about how modern drugs interact with vitamin D metabolism. By getting your level above 60 ng/ml, all you are doing is getting your level to where most lifeguards' levels are at the end of summer, to levels our ancestors had when they lived in the sun, to levels regular users of sun-tan parlors levels achieve, and most importantly, to levels where vitamin D's pharmacokinetics are normalized.

In the end, if you have cancer and your physician won't do a risk/benefit analysis, do it yourself. The risk side of that equation is easy. Both Quest Diagnostics and Lab-Corp, the two largest reference labs in the USA, report the upper limit of 25(OH)D normal is 100 ng/ml and toxic is above 150 ng/ml, so 60 ng/ml is well below both. The reason levels up to 100 ng/ml are published normals is because there is no credible evidence in the literature that levels of 100 ng/ml do any harm and because sun worshipers often have such levels. (If you don't believe me, go to the beach in the summer for one month, sunbath every day for 30 minutes on each side in your bathing suit, and go home and have a 25(OH)D level.) By getting your level above 60 ng/ml, all you are doing is getting your levels into the mid to upper range of laboratory reference normals. Little or no risk.

What are the potential benefits? It probably depends on a number of things. Did your cancer cells retain the enzyme that activates vitamin D? Many do. Did your cancer cells retain the vitamin D receptor? Many do. If your cancer cells get more substrate [25(OH)D], will that substrate induce the cancer cells to make more vitamin D receptors or more of the activating enzyme? Some cancer cells do both. In practical terms, vitamin D is theoretically more likely to help your cancer the earlier you start taking it. However, no one knows. Certainly there is no reason, other than bad medicine, for cancer patients to die vitamin D deficient. Unfortunately, most do.

Tangpricha V, et al. Prevalence of vitamin D deficiency in patients attending an outpatient cancer care clinic in Boston. Endocr Pract. 2004 May-Jun;10(3):292-3.

Plant AS, Tisman G. Frequency of combined deficiencies of vitamin D and holotranscobalamin in cancer patients. Nutr Cancer. 2006;56(2):143-8.

It is very important that readers understand I am not suggesting vitamin D cures cancer or that it replace standard cancer treatment. Oncologists perform miracles every day. Do what they say. The only exception is vitamin D. If your oncologist tells you not to take vitamin D, ask him three questions. 1) How do you convert ng/mls to nmol/Ls? How many IU in a nonogram? 3) How do you spell "cholecalciferol?" If he doesn't know how to measure it, weigh it, or spell it, chances are he doesn't know much about it.

All of the epidemiological and animal studies in the literature suggest cancer patients will prolong their lives if they take vitamin D. I can't find any studies that indicate otherwise. However, none of the suggestive studies are randomized controlled interventional trials; they are all epidemiological or animal studies, or, in the case of Vieth's, an open human study. However, if you have cancer, or your child does, do you want to wait the decades it will take for the American Cancer Society to fund randomized controlled trials using the proper dose of vitamin D? Chances are you, or your child, will not be around to see the results.

John Cannell, MD
The Vitamin D Council
9100 San Gregorio Road
Atascadero, CA 93422

This is a periodic newsletter from the Vitamin D Council, a non-profit trying to end the epidemic of vitamin D deficiency. If you don't want to get the newsletter, please hit reply and let us know. This newsletter is not copyrighted. Please reproduce it and post it on Internet sites. Remember, we are a non-profit and rely on donations to publish our newsletter and maintain our website. Send your tax-deductible contributions to:

The Vitamin D Council
9100 San Gregorio Road
Atascadero, CA 93422

PS: The Vitamin D Council lost our webmaster. If you want to donate your time to a good cause, know all about maintaining websites, are interesting in keeping up with the latest press about vitamin D, and are willing to do so for free, please hit reply and let me know. We currently have $405.52 in our bank account so we cannot pay you now but may be able to pay you in the future.

Let me explain what I mean by "genetic small LDL." I think it helps to illustrate with two common examples.

Ollie is 50 years old, 5 ft 10 inches tall, and weighs 253 lbs. BMI = 36.4 (obese). Starting lipoproteins (NMR):

LDL particle number 2310 nmol/L
Small LDL: 1893 nmol/L (1893/2310 = 81.9% of total, a severe small LDL pattern)

Stan is 50 years old, also, 5 ft 10 inches tall, and weighs 148 lbs. BMI = 21.3. Starting lipoproteins:

LDL particle number 1424 nmol/L
Small LDL 1288 nmol/L (1288/1424 = 90.4% of total, also severe)

Both Ollie and Stan go on the New Track Your Plaque diet and eliminate wheat, cornstarch, and sugars, while increasing oils, meats and fish, unlimited raw nuts, and vegetables. They add fish oil and vitamin D and achieve perfect levels of both. Six months later, Ollie has lost 55 lbs, Stan has lost 4 lbs. A second round of lipoproteins:

Ollie:

LDL particle number 1810 nmol/L
Small LDL: 193 nmol/L (193/1810 = 10.6% of total)

Stan:

LDL particle number 1113 nmol/L
Small LDL 729 nmool/L (729/1113 = 65.4% of total)

Ollie has reduced, nearly eliminated, small LDL through elimination of wheat, cornstarch, and sugars, along with weight loss, fish oil, and vitamin D.

Stan, beginning at a much more favorable weight, reduced both total and small LDL with the same efforts, but retains a substantial proportion (65.4%) of small LDL.

Stan's pattern is what I call "genetic small LDL." Of course, this is a presumptive designation, since we've not identified the specific gene(s) that allow this (e.g., gene for variants of cholesteryl ester transfer protein, hepatic lipase, lipoprotein lipase, and others). But it is such a sharp distinction that I am convinced that people like Stan have this persistent pattern as a genetically-determined trait.

Anonymous
4/3/2008 12:18:00 AM |

Thank you for this post. By the way, none of your links work because there's an extra http:// at the front. Same problem in previous posts as well.

phishery
4/3/2008 3:16:00 AM |

I have tried to centralize as much as I can about using a low carb / low glycemic approach which allows for low insulin diabetes management at http://www.dsolve.com. The site is free and has scientific research, recipes, as well as a "how to" course by a great doctor in the UK.

bob (the traveller)
4/3/2008 9:59:00 AM |

Extremely great post! As one who had gone through the low-card path (unguided by an expert but yet successful now into the 6th month) I can identify with a lot of the things mentioned here. I did not have the luxury of a mentor or a guide and so discovered a lot about sugar, carbohydrate and the body hands on and through research. But through it all, I'm glad that I now have a diploma in nutrition!

Peter
4/3/2008 12:10:00 PM |

I use the strips to test my blood glucose, but I don't know how high is too high.

Anonymous
4/3/2008 12:21:00 PM |

What an outstanding website. Jenny could be writing the books. She certainly has spent years researching this, and her approach makes sense. It's mind boggling to me that the ADA (American Diabetes Association) hasn't figured it out--that high carbs do not work. No wonder health care is so expensive in the US. Jenny's website gives anyone the tools to understand the sugar issues and take control themselves. Thank you for posting this.

Anne
4/3/2008 6:04:00 PM |

Zevia is a new, natural alternative to diet soda. All the flavors are carbohydrate and sugar free! There are no artificial sweeteners, flavors, or colors. Zevia satisfies my soda craving and allows me to avoid compromising my health with sugar and or artificial sweeteners such as Splenda. Stevia an ingredient in Zevia, is a herb native to central and South America and 200-300 times sweeter than sugar. Zevia is an excellent product for people diagnosed diabetes.

Anonymous
4/4/2008 1:21:00 AM |

I bought one of the newer glucose meters. The insert listed the readings that are still within normal on their meter, but they are higher then those listed as "normal." I don't know why there's a difference but the meter normal ranges are higher.

Anonymous
4/5/2008 1:29:00 AM |

My story is ditto to yours Jenny. I started with Atkins, upset all my docs and was scolded even though got off insulin and statins. No support except atkinsdietbulletinboard.com but I was one of the leaders there on diabetes so didn't really have a mentor.

I was a reborn again lo carber and was rigid for 3 yr and have fallen a few times, but like you have found a way to try stay within the norms and eat to my meter.

As I age I need to eat less and work harder.
Peter the norms I aim for are under 6.1 . However, that is not always attainable.

Thnx Jenny for taking the time to write.Too bad nutritionists, diabetologists ect weren't as educated as us patients.

chick

Jenny
4/6/2008 2:39:00 PM |

Thanks for the kind words! And thanks to everyone who visited the site from this blog. Obviously there are a lot of people reading here!

The "normal" range that came with your meter is probably the one defined by the American Association of Clinical Endocrinologists. They currently recommend that people with diabetes get under 140 mg/dl (7.7 mmol/L) at 2 hours.

This, however, is FAR from normal if we use CGMS studies of normal people's post meal response to define normal.

This is discussed in detail on my web site on THIS PAGE.

Red Sphynx
4/9/2008 5:07:00 AM |

Jenny is wonderful. I'm thinner and healthier today because of the excellent advice at alt.support.diabetes; starting more than five years ago. And Jenny was always one of the best.

Adam Becker Sr.
5 years in the 5% club, thanks to Jenny, Jennifer, Quentin, several Alans, Jefferson and more.

jpatti
4/28/2008 9:19:00 PM |

I agree with sphynx, I'm a big Jenny fan also!

Anonymous
6/5/2008 6:21:00 PM |

re: exercising to burn off carbs

i understand the point about burning calories and utilizing blood glucose and glycogen stores and such... but i've always understood from sports nutrition research that most of us should eat carb-rich foods after exercise. i thought that carbs before exercise is generally just to keep you going through the workout...

cymoore
7/1/2008 8:54:00 AM |

Thanks for the detailed and thoughtful post. In response to anonymous, I don't believe that carbs are ever really "necessary", and in any case, it's hard to avoid them entirely. I've been low carbing for 6 months now (lost ~18 lbs) and run/hike a lot. Even after a 16 mile trailrun covering a couple thousand feet elevation, my blood sugar was 94 (without eating any carbs during the exercise). I guess the body is just very good at supplying glucose even if you don't eat carbs (gluconeogenesis from pyruvate). Supplementation with branched chain amino acids might be helpful since these are broken down during endurance exercise and need to be replaced, but I see no evidence that carbs are needed. Still,carbs are better tolerated when people exercise because insulin sensitivity is increased.

Healthy Womens
10/3/2009 3:22:37 AM |

[...]There are plenty of information and tips about the low carb diet recipes. No matter what sources of information or tips you choose you need to always keep in your mind that the low carb diet recipes should consist of healthy and match with your diet plan[...]

buy jeans
11/3/2010 6:41:54 PM |

Unlike much of what you've read before, there are no scholarly references for this section. It's based entirely on my own observations and the experience of many dozens of people who have participated in online discussion groups devoted to low carb dieting and diabetes.

Neelesh
12/6/2007 3:25:00 PM |

Dr Davis,
I'm unable to get Vitamin D3 (cholecalciferol) in India. What is being sold is calcium + Vitamin D3 or Alfacalciferol or Calcitriol (http://en.wikipedia.org/wiki/Calcitriol).
While I couldn't find much about alfacalciferol, Calcitriol's composition looks very similar to what you describe.
I wonder if they are the same.
-Neelesh

Anonymous
12/6/2007 5:02:00 PM |

Dr. Cannell's arguments make a lot of sense, but his statement that "If he doesn't know how to measure it, weigh it, or spell it, chances are he doesn't know much about it." would carry more weight if he hadn't misspelled nanogram in the immediately preceeding sentence.

g
12/6/2007 9:48:00 PM |

I like the Feng Shui or symmetry of 60-60-60-60....

Actually it's 60-60-60-60-60 if you include Apolipoprotein B...
(although I know you are achieveing TGs<45!)

This is great! Thank you, g

TedHutchinson
12/7/2007 12:21:00 AM |

Those readers who want to check what the research papers actually said may find the NUMBERS that I have emboldened useful. If you just cut and paste the darker number into the search-box at pubmed it should bring up the right paper.
Moan J, et al. Colon cancer: Prognosis for different latitudes, age groups and seasons in Norway. J Photochem Photobiol B. 2007 Sep 19 18029190
Lagunova Z, et al. Prostate cancer survival is dependent on season of diagnosis. Prostate. 2007 Sep 1;67(12):1362-70 17624920
Porojnicu AC, et al.  Changes in risk of death from breast cancer with season and latitude: sun exposure and breast cancer survival in Norway. Breast Cancer Res Treat. 2007 May;102(3):323-8.17028983

Porojnicu A, et al.  Season of diagnosis is a predictor of cancer survival. Sun-induced vitamin D may be involved: a possible role of sun-induced Vitamin D. J Steroid Biochem Mol Biol. 2007 Mar;103(3-5):675-8. 17229569

Porojnicu AC, et al.  Season of diagnosis is a prognostic factor in Hodgkin's lymphoma: a possible role of sun-induced vitamin D. Br J Cancer. 2005 Sep 5;93(5):571-4.17229569

Lim HS, et al.  Cancer survival is dependent on season of diagnosis and sunlight exposure. Int J Cancer. 2006 Oct 1;119(7):1530-6.16671100

Zhou W, Vitamin D is associated with improved survival in early-stage non-small cell lung cancer patients. Cancer Epidemiol Biomarkers Prev. 2005 Oct;14(10):16214909
Berwick M, et al.  Sun exposure and mortality from melanoma. J Natl Cancer Inst. 2005 Feb 2;97(3):195-9.15687362
Tangpricha V, et al.  Vitamin D deficiency enhances the growth of MC-26 colon cancer xenografts in Balb/c mice. J Nutr. 2005 Oct;135(10):2350-4.16177194

Schwartz GG, Skinner HG. Vitamin D status and cancer: new insights. Curr Opin Clin Nutr Metab Care. 2007 Jan;10(1):6-11.17143048

Woo TC, et al.  Pilot study: potential role of vitamin D (Cholecalciferol) in patients with PSA relapse after definitive therapy. Nutr Cancer. 2005;51(1):32-6.15749627

Hollis BW, et al.  Circulating vitamin D3 and 25-hydroxyvitamin D in humans: An important tool to define adequate nutritional vitamin D status. J Steroid Biochem Mol Biol. 2007 Mar;103(3-5):631-4. 17218096

Tangpricha V, et al.  Prevalence of vitamin D deficiency in patients attending an outpatient cancer care clinic in Boston. Endocr Pract. 2004 May-Jun;10(3):292-3.15310552

Plant AS, Tisman G.  Frequency of combined deficiencies of vitamin D and holotranscobalamin in cancer patients. Nutr Cancer. 2006;56(2):143-817474859

I just feel so upset that I have been misinterpreting Hollis's paper Circulating Vitamin D3 and 25-hydroxyvitamin D in Humans and been telling people that 100nmol/l was a reasonably safe minimum. Looking again at those figures 1 and 2 I take Cannell's point that it may be better, safe rather than just stopping at 40ng 100nmol/l it may be safer, allow a bigger margin for error, to consider 50-60ng/ml 125nmo/l- 150nmol/l as the range for optimal health.
It's bad enough taking the flax and suggesting 4000iu/d is safe and reasonable where no sun exposure is possible.
I suspect I'm going to be even more unpopular suggesting 7000iu may be necessary in some/many cases.

Anonymous
12/7/2007 4:47:00 AM |

Is there any danger from Vitamin D levels that are close to the upper ends of the 'safe' spectrum?

A study in India once linked high D levels (89 ng/mL) to higher incidents of cardiac disease, but that study was a bit iffy.

Info can be found here: http://www.westonaprice.org/basicnutrition/vitamin-d-safety.html

Although the reference to the Indian study is buried a bit deep in that page. A lot of info there though.

Dr. Davis
12/7/2007 11:46:00 AM |

What an excellent summary!

You can see that data probing the health effects, or detrimental effects of higher levels of vitamin D3 (as 25-OH-vitamin D3) are poorly explored. We aim for a blood level of 50-60 ng/ml and have observed no toxic effects whatsoever. In fact, we've observed positive effects well beyond our expectations.

Nonetheless, I think that going above 60 or 70 ng/ml is relatively uncharted territory.

TedHutchinson
12/7/2007 5:34:00 PM |

http://www.vitamindcouncil.com/worst_science.shtml This summary of the Indian research mentioned earlier may help those who are unfamiliar with what is being discussed here.

The problems associated with standardisation of scores between different assessment records is complex and discussed in this paper. Serum 25-hydroxyvitamin d measurement in a large population survey with statistical harmonization of assay variation to an international standard.
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17726070 There was pre-publication full text pdf version online, with some nice charts of UK vitamin d status through the year at the back, but I cannot find it now.

There is still a problem between different assay methods and lab accuracy as some of the presentations at this conference make clear.
http://app2.capitalreach.com/esp1204/servlet/tc?cn=asbmr&c=10169&s=20343&e=6950&&
The http://www.deqas.org/ system for ensuring a world standard.

While of course we must not totally turn our back on past research we do have to consider whether the levels reported would stand comparision with current standards of assessment.

While I am not suggesting that anyone should try this at home.
Safety of vitamin D3 in adults with multiple sclerosis used progressively increasing doses of vitamin D3: from 700 to 7000 microg/wk (from 28000 to 280000 IU/wk). I personally believe Vieth to be an honourable man who would, should adverse events have been record would have reported them.
Such very high dose levels are outside of the scope of "NORMAL" vitamin D supplementation but the very fact that when tested, the results have been predictable, does give us confidence thatRisk Assessment for Vitamin D
http://www.ajcn.org/cgi/content/full/85/1/6 does stand up to scrutiny when tested.

In order to reach the levels detailed by Hollis in Circulating Vitamin D3 and 25-hydroxyvitamin D in Humans: those particularly living above latitude 37 are going to have to use more Vitamin D than Krispin Sullivan suggests during the winter months when sunlight is unavailable. It's my view that the risks associated with low vitamin d status are higher than the alleged, unproven risks of supplementing with up to 10,000iu/daily though in practice a total intake of 4000 -7000iu appear to be required during the winter when sun/uvb is not an option.

Vaughny
12/8/2007 1:23:00 AM |

Good material on Vit D. He mentions monthylu blood calcium tests - how critical is this test if one were supplementing in the 4000IU - 6000IU / day range? Would Vit K2 help prevent higher blood calcium?

Dr. Davis
12/8/2007 1:26:00 AM |

Monthly calcium tests are silly. There is absolutely no need for this in 99.9% of people.

No, vitamin k2 will not prevent a rise in calcium. The worry that vitamin D will raise calcium is, for the extreme majority, unfounded.

Mo
12/8/2007 11:33:00 PM |

Isn't it actually possible that from a certain level of D upwards, that D keeps calcium from not only getting too low but also too high?

If your D is low I'd imagine your blood calcium would at first be high or within the upper limits of normal before going on a possible plummet route if your D drops more.

I guess once D has satisfied your bones, it doesn't over do it and distributes to other needy areas.

Thomas
12/9/2007 9:48:00 PM |

Will any fat (nuts) have similar results compaired to olive oil?

How often should blood tests be necessary to test vitamin-d absorption ?

Coulden't find answers to these questions using Google or Dr. Cannell's web site.

Dr. Davis
12/9/2007 11:07:00 PM |

I don't know. I suspect they have some effect, but I've not examined it specifically.

We check our patients every 6 months.

buy jeans
11/3/2010 10:31:11 PM |

While cancer is not our focus on the Heart Scan Blog, Dr. Cannell's always insightful comments provide some helpful thoughts for our management of vitamin D doses and blood levels.

John F Ocel JR
10/13/2011 5:38:58 AM |

DR Carnell im a huge fan of you and i know ur very smart and good at what u do and love to help educate people about there health expecially about vitamin d i am 28 years old 290 pounds 5 foot 10 vitamin d defient and have severe hypertention i take tribenzor 40-10-25 mg's in the am and monopril 20mg's in the pm, and b12 sublingual which works wonders for me mentally well anyways since iveb been taking bob barefoots coral calcium and vitamin d 3 my blood pressure went from 125 70 to 88/37 i felt like crap i stopped the tribenzor 40-10-25mg pill and increaded the monopril to 30 mg;s my pressure has been 126/60 im feeling a feverish warm feeling i wonder if its the vitamin d 3 or coral calcium or too much b12 or could it be the withdrawals of tribenzor is a cobination drug 3 pills in one for hypertention i took alil less then half a pill of the tribenzor and the fever hot flashes went away my doctor already told me that vitamin d doesnt lower bloodpressure so what should i do and what should i say to him i have an appointment the 25th of october for a bloodpressure check up. Please help me fit the batlle of hypertention and give me ur honesy opinion thanks doc god bless u were put on this earth to help people like me thnak you. Just wanted to let u know im taking about 5,800 ius a day thank you.and also when i stop the monopril ive had heart fluttering ive done it before, been on it since i was 16 years old.

Onschedule
2/18/2010 8:25:54 PM |

Your blog entry appears to have been truncated.

Anonymous
2/18/2010 8:29:46 PM |

How are Stan's blood sugars?

zach
2/18/2010 8:59:48 PM |

Sounds like Stan is screwed. Of course, there may be other factors mitigating his lipid pattern because he avoids the neolithic agents. Stan would be more susceptible to heart disease than ollie on the SAD, but not when they both have good diets?

Jeff
2/18/2010 10:23:31 PM |

Is it possible that a different diet might work for Stan? I don't know what it would be, I just wonder if it's possible.

Kurt G. Harris MD
2/18/2010 10:29:07 PM |

So Ollie and Stan BOTH show substantial improvement on their LC diets.

The difference between them may well be due to genetics, but where is the evidence that Stan needs to avoid saturated fat?

Did you advise Stan to increase sat fat and then watch his sdLDL get worse?

If they accomplished this with "oils" at the expense of saturated fats (oils are liquid due to the paucity of saturated fats in them), then it looks like they both have a saturated fat deficiency, and one could speculate that Stan is even more deficient than Ollie.

Swap out the nasty oils for more butter and beef fat and coconut fat and maybe Ollie will have sdLDL of 0 (like I do on 35% of calories from sat fat) and Stan will improve even further.

Peter
2/18/2010 10:44:33 PM |

Hi Dr Davis,

You describe a fascinating scenario.

Ollie has clearly lost weight. He has lost 55 lb in 6 months. That is nearly 10 pounds of "lard-equivalents" each month. This has not evaporated. It is exactly what he has been running his metabolism on. Whatever nuts and vegetables he has eaten can have been nothing in comparison to the 4 times half pound blocks of lard he has "eaten" from his own adipose tissue, every week. Result: Metabolism runs on lard and sdLDL plummet.

Stan has lost minimal weight so has run his metabolism on his food alone. If this is low in lard he may well be running his metabolism on vegetable derived carbohydrate and nut derived omega 6 PUFA. It's possible he has NOT been eating 2lb of lard a week in his diet, because obviously this might raise his LDL. So he has NOT used lard to fuel his metabolism, he has used nuts and vegetables when Ollie has used lard from his adipose stores.

Before I would blame genetics I would get rid of the nuts and unlimited vegetables from Stan's diet and replace them with exactly the same the adipose tissue derived fuel that Ollie was using. If Stan cannot spare it from his butt (he certainly cannot at BMI 21), it's going to have to go on his plate. Two pounds of lard a week.

Then compare sdLDL values, when you have similar metabolic situations... Until then Stan just has nut and vegetable poisoning showing as sdLDL.

There do not have to be any genetics involved. There might be, but let's keep it simple for the time being... Ollie is on lard while he is losing weight. Mimic that.

Peter

Sue
2/18/2010 11:16:15 PM |

Stan did improve. Maybe he will improve further, the longer on diet?

Anonymous
2/18/2010 11:52:16 PM |

I think it's somewhat telling that you advise your patients to eat "oils." What kind of "oils" are they eating? Why are your patients eating unlimited nuts?

Until you get off the Omega-6-loaded "heatlhy" polyunstaturated fats bandwagon, it's hard to take your clinical observations on "fats" very seriously.

stcrim
2/19/2010 12:15:07 AM |

Dr. Davis,

Help me understand the part about not eliminating meats or fats.  First, here is my blood work 15 days apart.

Total cholesterol 295 - 15 days later 156
LDL 200 - 15 days later 102
HDL   46 - 15 days later  32  (have added 1500mg of niacin since then)
Triglycerides   242 - 15 days later 109
VLDL  49 - 15 days later 22
Vitamin D was 28 â€“ 15 days later itâ€™s 56 (using 10,000 of Carlsonâ€™s D3)

FYI my heart scan was 899 (54 year old male)

I started on all the main nutrients you recommend here plus a few.  I dropped dairy like a hot potato including 6 or more ounces of cheese a day.  During those 15 days I ate only plant based foods (have since added some salmon and egg whites)

The only oil I use now (sparingly) is olive.  I have a couple of gallons of coconut oil I assumed would have to be tossed sooner or later.

Guess you could say I became fat paranoid and downright phobic about any saturated fat.

Am I understanding I could add back Grass-fed beef (omega-3) pastured chicken and Omega-3 whole eggs?  Coconut oil?   If so, is there some safe percentage of a personâ€™s diet to include those proteins/fats?

By the way, my doctor wouldnâ€™t let me out of his office without a copy of your book.  Heâ€™s one in a million as are you!

Steve

Daddy
2/19/2010 1:05:49 AM |

Doc, would you say family history could be a clue towards small-particle tendencies? I have zero family members with heart issues yet I was given pause by your recent post on saturated fats having a disproportionate affect on these genetically challenged folks. I ask because I eat a ton of rib eyes and bacon.

Dr. William Davis
2/19/2010 3:08:19 AM |

I have indeed had many people with presumed "genetic small LDL" load their diets with oils and fats with only minor improvement. Loaded with saturated fat, however, and there seems to be deterioration.

I know this flies in the face of the "saturated fat is great" dogma, but I don't make this stuff up. Just as I don't make up the deterioration of postprandial triglycerides and chylomicron remnant effect when saturated fats are loaded heavily in the diet.

The persistence of small LDL is also long-term, i.e., it persists for years despite continuing efforts.

Dr. William Davis
2/19/2010 3:09:48 AM |

Oils = olive oil, flaxseed oil, canola oil (yes, yes, I know), avocado, almond, oils from raw nuts and meats.

No polyunsaturates here. You've go the wrong guy.

Richard A.
2/19/2010 3:41:23 AM |

On Doctor's orders, Ollie did indeed lose a massive amount of weight.
http://www.youtube.com/watch?v=IYAeYj8-G4w

LynP
2/19/2010 3:41:52 AM |

@Peter, fascinating...eat lard when slim in attempt to reduce sdLDL. Doc D thanks for 'splaining 'genetic' tendency to sdLDL & why numbers not reduced on sat fat & only reduced mildly on mono sats. Great info guys!

Kurt G. Harris MD
2/19/2010 3:52:12 AM |

"Oils = olive oil, flaxseed oil, canola oil (yes, yes, I know), avocado, almond, oils from raw nuts and meats.

No polyunsaturates here. You've got the wrong guy."

But Dr. Davis, those all chock full of PUFAs

Linseed oil (flax oil) is 71% LA and ALA

Rapeseed oil (Canola oil) is 33% LA and ALA

Almond oil is about 25% PUFA

Even olive oil can be up to 20% PUFA

And all of these are mostly Linoleic acid.

All best left as industrial lubricants and paint additives rather than eaten.

LeenaS
2/19/2010 4:10:32 AM |

So, you have a fat guy, who has been living on (his own) saturated animal fats, and he has improved a lot.

Then you have a skinny guy, who has been living on "healthy vegetable fats" with surprisingly much LA in them, and he has not improved that much.

So, it seems to tell that without saturated fats LDL improvement is much harder in LC, to say it kindly.

And it sounds as if butter and saturated animal fats would be advantageous for the latter guy, too. Have they ever tried this, under your coucelling?

With regards,
LeenaS

Anonymous
2/19/2010 4:30:07 AM |

Dr. Davis,

While body composition certainly isn't a prerequisite for being part of a classic comedy team, I couldn't help but notice that Stan had the makings of a skinny-fat bean pole checking in at 5' 10" and only 148 pounds. Those stats make him sound like a diehard distance runner or a chain smoker.

While it was clearly just for illustrative purposes, I couldn't help but think that, if "Stan" exercises at all, he must not be exerting himself very much. I'm not advocating that every older gentleman suddenly attempt to impersonate Mr. Olympia, but I have to wonder seeing such a lightweight. That's not to say that I think sufficiently intense exercise would remove the problem that is genetically-based small LDL, but it is enough to make me raise an eyebrow when I see that type of weight for a male listed as 5'10".

Anonymous
2/19/2010 4:32:12 AM |

Dr. Davis,

Would a take-home point simply be to let the numbers from proper testing be the guide versus what we "think" is right based upon generally-sound dietary advice that may apply to many, but not all, situations?

Bill Lindvall

Anonymous
2/19/2010 7:25:27 AM |

Olive oil is monounsaturated but flaxseed oil, canola oil, avocado oil, almond oil, and oils from raw nuts are all polyunsaturated oils! Yes, flax oil is omega 3 and canola has more omega 3 than omega 6, but both omega 3 and omega 6 are polyunsaturated.

Sue
2/19/2010 8:10:06 AM |

Do you know how much saturated fat was eaten?

Sue
2/19/2010 8:28:08 AM |

Maybe too much mono-unsaturates?

Anonymous
2/19/2010 11:18:48 AM |

In another post, you said that blood sugars parallel small LDL. Do Stan's blood sugars follow the pattern you would predict for someone with a lot of small LDL?

http://heartscanblog.blogspot.com/2009/12/to-track-small-ldl-track-blood-sugar.html

lightcan
2/19/2010 12:46:27 PM |

No polyunsaturates?
Because olive, flax, canola oils, nuts have no polyunsaturated fats?
I found something different.
Even avocados have 10 % PUFAs.
http://curezone.com/foods/fatspercent.asp

Anonymous
2/19/2010 2:01:52 PM |

So what about epigenetics? Any way to modify this unknown gene or set of genes? Pomegranate, etc?

Adolfo David
2/19/2010 2:27:14 PM |

Please guys, find so other monounsaturated (MUFA) fats with less PUFA..

I eat almonds, walnuts, extra virgin olive oil as fats and my diet is low in Omega 6, 10% or 20% of Omega 6 PUFA is nothing compared with 70 or 85% of MUFA.

My experience taking a lot of saturated fats with low carbs is bad, I prefer a diet high in MUFA and low carb.

Anonymous
2/19/2010 3:18:19 PM |

Maybe the mental stress of having to worry about what to eat is a factor.
I do find my self stressing about that often and wonder if just enjoying the food would give me a longer nicer life quality which is in then end what matters.

Which reminds me somehting I have never read in this blog is about cortisol.
Have you ever tracked cortisol levels in your patients?

ET
2/19/2010 5:37:36 PM |

A yea ago, i went off niacin and zocor due to elevated liver enzymes. Before I restarted niacin, an NMR lipoprotein analysis showed:
LDL particle number - 2197
Small LDL-P - 1614
LDL Particle size - 20.3
Saturated fat (% of calories) - 21%

Six months later, after radically increasing the amount of coconut oil I consumed, the results were:
LDL particle number - 896
Small LDL-P - 466
LDL Particle size - 21.6
Saturated fat (% of calories) - 45%

Five months after that:
LDL particle number - 946
Small LDL-P - 120
LDL Particle size - 21.1
Saturated fat (% of calories) - 52%

Carbohydrate consumption has held fairly steady at 10% of calories.

Vladimir
2/19/2010 5:41:33 PM |

I agree 100% with these comments.  Not a drop of dogma in them; pure science.  Yes, omega-6 is evil; avoid foods with any of it. No nuts, no seeds. Soy -- dangerous.  Milk -- cavemen didn't drink it and it's possibly dangerous too.  Vegetables -- no, no, goodness no, they're mostly made of dreaded carbohydrates, have little fat, an fiber isn't important!  Saturated fat?  I don't know about you, but I'm too scared to go hog wild on it.

I know, I know!  Let's not eat at all.  That would drive small LDL to 0!  That would end heart disease -- and everything else -- in a flash.

Or, just maybe, we could be moderate and sensible.  Take some fish oil to balance whatever omega-6 you get in the olive & canola oils and in nuts.  Eat some, but not too much, animal protein, and mostly fish and lean meats at that, because saturated fat isn't out of the woods yet. (Just because saturated fat's risks have been over-hyped doesn't mean that we should eat all meat all the time, because the evidence is not in yet that saturated fat is a panacea.) Eat some, but not tons, of fruits, because they have antioxidants.  And for goodness sake, eat your vegatables -- lots of them, and all kinds of them -- because your mother was right to make sit at the table until you finished them.

Anonymous
2/19/2010 5:51:09 PM |

"I couldn't help but notice that Stan had the makings of a skinny-fat bean pole checking in at 5' 10" and only 148 pounds. Those stats make him sound like a diehard distance runner or a chain smoker."

I'm 5'10" and under 145 lbs., and I'm neither.

Anonymous
2/19/2010 6:15:07 PM |

Kurt G & Lightcan,

I think when Dr. D said no "No polyunsaturates here. You've got the wrong guy."...he probably meant to say "No (high omega 6) polyunsaturates here.".

Lastly...I have a question for Dr. Davis:

Dr. D., is this "genetic small LDL" the same as when you talked about people with ApoE4 in your November 17, 2008 post? If so, do you think it would be helpful to test ApoE before experimenting with diet??

Thanx!

John M.

zach
2/19/2010 6:20:59 PM |

Aren't most nuts full of N-6 PUFA?

Rainer
2/19/2010 6:23:53 PM |

Hi Dr. Davis,

and what is happend with the triclycerides of Stan. Are they high too?

Anonymous
2/19/2010 7:14:40 PM |

This is usually when the good doctor stops answering comments.

Come on, Dr. D, prove me wrong!

Anonymous
2/19/2010 7:24:49 PM |

You have really great taste on catch article titles, even when you are not interested in this topic you push to read it

Donny
2/19/2010 7:33:02 PM |

I'm going to steal a page from T. Colin Campbell here (yechh!)

Dr Davis, you say that

"I have indeed had many people with presumed "genetic small LDL" load their diets with oils and fats with only minor improvement. Loaded with saturated fat, however, and there seems to be deterioration."

Campbell makes the contention that studies showing that low saturated fat intake is beneficial (never mind whether they actually exist or not, just for the sake of argument here) might actually have nothing to do with the type of fat in the diet, and everything to do with the protein which accompanies the fat; most animal fat in our culture comes attached to meat (protein.)

Adding plant fats and oils to the diet, including nuts, would tend to increase total percentage fat in the diet at the expense of both carbohydrate and protein. Adding animal fat, attached to meat might increase total protein percentage even as it increases total saturated fat.

Understand, I'm not saying "protein bad," I guess I'm just echoing Peter, really, Stan may be trying to live off of a protein/fat mix that's too rich in protein, entirely aside from the whole issue of saturation.

Jeanie Campbell
2/19/2010 7:57:39 PM |

Don't tell me no one picked up on the Laurel and Hardy reference! Brilliant!

Anonymous
2/19/2010 10:16:49 PM |

Could all you saturated fat mafia people please stop polluting the comments section?

Sue
2/20/2010 12:48:15 AM |

Maybe recommend Stan use only sat fats and no poly oils and then see if there is a change.

Anonymous
2/20/2010 2:29:41 AM |

Drs. Davis and Harris,

Googlemaps indicate you two practice your medicinal arts about 154 miles away from each other.

May I respectfully suggest a summit meeting in Manitowoc to resolve these matters?

Scott Miller
2/20/2010 3:31:43 AM |

Flax oil, canola oil, any nut oil (except macadamia nut oil), and all of those nuts -- these are all rich with polyunsaturated fats. I never eat these oils, and my Lp(a) is 2, as last measured a few months ago.

I always recommend nuts as a very moderate snack because of their high PUFA content. Macadamia nuts are the ONE exception, with a fatty acid profile similar to olive oil. Basically, I never recommend any food with a PUFA content greater that 12 percent. That means canola oil is right out!

Dr. Davis, perhaps try putting a few of these presumed "genetic small LDL" people on a real low PUFA diet for a while (with more coconut oil and butter--but no nuts during this period) and see if there's improvement.

I'd bet there is. Nothing really to lose by giving this a shot.

If it works to your satisfaction, I'll donate $1000 to your Track-the-Plaque program, or a charity of your choice.

Dr. William Davis
2/20/2010 1:58:33 PM |

Some other features of the presumptive "genetic small LDL" pattern:

1) It occurs in the minority of people with small LDL, likely less than 20% of people who start with substantial small LDL.

2) It is associated with insulin resistance and a tendency towards diabetes

3) It can occur independent of ApoE genotype. However, if it occurs with ApoE2, it means a very potent carb-sensitivity/diabetic tendency.

4) The "floor" of 600 nmol/L can be broken. We've had success achieving really low body weight and inconsistently with several supplements, e.g., phosphatidylcholine.

This area is fascinating, though very poorly explored. "Genetic small LDL" is truly one of the problem areas in gaining control over heart disease risk.

Henry North London
2/20/2010 2:23:56 PM |

I currently consume coconut oil and butter  I do not use any lard or pufas  I consume a moderate amount of almonds a day ( nine) and some ground almonds as a meal replacement about 10-20gs as a meal about two or three times a week

I eat avocados maybe twice a week  about two-three

I have started to show my abdominal muscles after two months where before I looked as if I were pregnant of about a 5 month pregnancy

I have dropped half a stone  My BP is controlled by a sartan

I consume a moderate amount of frozen blueberries and raspberries May be about 1 kg of each a month

or less

I am living on saturated fat and loving it

My body works better on it but then I have blood group B

You have to eat right for your blood type perhaps?

Miki
2/20/2010 3:17:30 PM |

I would like to add support to Dr. Harris' hypothesis. LDL (no NMR in our country) and TG both rise on low carb, high sat fat diet. No weight problem ever. No high protein no high PUFA for me. Pre-diabetic fasting glucose (110-120). Only complication is I had my gallbladder removed (but my brother didn't). Will increase coconut oil and olive oil on account of double cream. Feel so good on low carb it can't be wrong. Also wonder if under healthy low carb diet LDL and TG have atherogenic effect (My calcium score is low)
In summary I think Dr. Davis is onto something but I would love to know if LDL status corresponded to increased calcium score in the said patients.

Donny
2/20/2010 3:41:44 PM |

Choline deficiency can lessen hyperglycemia in rodents with fatty livers. Maybe the inconsistent effects of phosphatidylcholine have something to do with that?

To the person who mentioned the saturated-fat mafia; we have limited information going in here. Trying to guess at alternate explanations isn't the same as insisting that saturated fat is good in all situations for everybody, no matter what. Proper skepticism demands that we question even the most respected sources.

Anonymous
2/20/2010 8:12:29 PM |

Dr. Davis, this recent article seems congruent with some of your observations:

http://jn.nutrition.org/cgi/content/abstract/jn.109.115964v1

Anonymous
2/20/2010 8:16:01 PM |

To all these nutty omega-6 fatphobes - I eat lots of nuts of all sorts, probably 40% of calories, including... peanuts, which I am aware are a legume. I have no small LDL, undetectable CRP, and lp(a) of 4, high hdl and low homocysteine, HbA1C of 5.2.

Anonymous
2/20/2010 9:06:44 PM |

Dr. Davis,
You said "Some other features of the presumptive "genetic small LDL" pattern:

1) It occurs in the minority of people with small LDL, likely less than 20% of people who start with substantial small LDL."

So, based on a minority of people with small LDL, you are recommending the same diet to everyone?

Dr. William Davis
2/21/2010 2:28:39 AM |

Please don't misunderstand: I am NOT saying that saturated fat increases small LDL in most people.

What I am suggesting is that there is a genetic minority in which saturated fat increases small LDL. These people seem to be the unusually slender, high HDL, low triglycerides, yet diabetes-prone who show apparently intractable small LDL.

I don't know for a fact why this happens, but I speculate that it is a genetically-determined trait.

This pattern responds best to a high-protein, high-fat, very low-carbohydrate diet. But saturated fat is the exception in this group.

Kurt G. Harris MD
2/21/2010 3:25:37 AM |

Hello Dr Davis

I am only persisting in this as the implications might be important.

I asked, "Did you advise Stan to increase sat fat and then watch his sdLDL get worse?"

You later said, "Loaded with saturated fat, however, and there seems to be deterioration." and ..

"What I am suggesting is that there is a genetic minority in which saturated fat increases small LDL."

and...

"This pattern responds best to a high-protein, high-fat, very low-carbohydrate diet. But saturated fat is the exception in this group."

Can I assume when you say "seems to be deterioration" and "there is a suggestion that saturated fat increases small LDL" and "saturated fat is the exception" that this is based on the observation of serially increased sdLDL NMR values after increasing only saturated fat intake in these 100 or so patients?

If this is what you have, serial NMRs that show increased sdLDL with increased saturated fat intake, why not say so explicitly?

Or is it just a reasoned (perhaps correct, perhaps not) guess of what would happen to sdLDL in those 100 or so who have this presumed genetic pattern of persistent sdLDL?

Rick
2/21/2010 3:24:07 PM |

Dr. Davis wrote:

"I know this flies in the face of the 'saturated fat is great' dogma, but I don't make this stuff up."

The way that Peter described the scenario you presented, it seems to support the health benefits of saturated fat rather than deride them

Ollie is mainlining saturated fat from his gut. Stan is not. Ollie's sdLDL drops like a rock. Stan's doesn't.

It seems like if this phenomenon of high sdLDL specifically affects low BMI people, their lack of saturated fat intake, whether through their mouths or from their love handles, could be the culprit.

kilton9
2/24/2010 10:45:35 PM |

Dr. Harris,

I'm a fan of your blog, but I can't help but notice that you have completely ignored Dr. Harris's questions in this entry as well as the other recent entry about saturdated fat and LDL. I find his questions to be pertinent.

bovinedefenestration
2/27/2010 7:26:50 AM |

I'm actually a little surprised no one's brought up this blog, that indicates polyunsaturate consumption over 4% of calories can be detrimental:

http://wholehealthsource.blogspot.com/2009/05/eicosanoids-and-ischemic-heart-diseas.html

Eh. Took me long enough to find. At any rate, 10-20% polyunsaturates, especially if they come from omega-6, is a huge amount for a human.

Imma going to go away and let you argue now.

Henry North London
2/27/2010 7:07:21 PM |

Hear Hear throwing cows out of windows... It blows the polyunsaturates out of the window

I have the printout of the Rose et al Paper..

Corn oil increased the death rate

Janet -Mich
2/28/2010 11:16:20 PM |

My family has a history of high colestral and plaque build-up in the blood. Should I stay on my Lipator and stay on a low-carb diet ? Your article brings up some red flags for me. Maybe I should talk to my Doctor, but my low-carb friends tell me the doctor will tell me to get off the diet ! I would like some advice.

dining table
7/9/2010 9:52:12 AM |

How did that happen? Is it possible? Different diet will work to Stan? I am curious about that. I will visit this blog again. I am hoping for an update.

Derek Weiss
8/4/2010 9:49:11 PM |

Obviously another great blog about eating and living right, but at some point we have to take a step back and live.  Food avoidance and constant stressing about food seems it could negate any benefits of just eating a sensible, well balanced, moderately low carb diet.

To me, all these nutrition blogs are fun to read at work. But have you ever noticed the incredible difference in opinion from one to the next?  I take all that with a large grain of salt, pun intended.

Oh my god, I ate a walnut, surely I will be in the cath lab tomorrow getting my LAD stented;)

You might not find yourself in the cath lab from eating the random 1/2 cup of oatmeal, but you might find yourself there from stressing about it too much.

Read all the blogs, use all the information to help guide you.  But don't get in line with the zombies and wander off the deep end too far.

Just a thought.

Liz Stanley
9/16/2010 8:32:32 PM |

Here's a stumper. I just had my VAP done and the results surprised me. Some background: I'm not on any medication and never have been. Never had a weight problem, body fat below 20%. I exercise regularly (CrossFit 4x/week). Never smoked. Rarely drink. I eat mostly a primal diet w/plenty of grass-fed/organic/cage-free/wild-caught meat/fish and lots of fresh veggies. Some dairy, but only hormone and antibiotic free. Hardly any grains or processed foods. Low fasting blood sugar (76 as of two weeks ago.) Here are my VAP results:

Total cholesterol: 200
HDL : 79
LDL: 106
VLDL: 14
Lp(a): 7
Triglycerides: 43

With all that I'd expect to have Pattern A LDL. Yet the VAP test says I have Pattern B! I'm not aware of any history of heart disease on either side of my family. But if it's true that my LDL is small and dense, all I can figure is that it must be genetic. I'm not really sure what to make of it! Any ideas?

Anonymous
9/24/2010 10:26:37 PM |

Liz Stanley - while my HDL and LDL aren't as good as yours (63 and 185 respectively), I also just received VAP results that stumped me for a similar reason. I exercise frequently, am not overweight, don't smoke or drink, eat low carb, etc., yet I have pattern B as well. To add to the confusion, my cCRP is 0.7, which my doctor said was excellent and basically renders my test results a wash as I have zero other risk factors. I don't know what to make of any of this when you put it all together, and I stumbled upon this post because I'm hoping to find some answers online.

buy jeans
11/3/2010 6:33:42 PM |

While body composition certainly isn't a prerequisite for being part of a classic comedy team, I couldn't help but notice that Stan had the makings of a skinny-fat bean pole checking in at 5' 10" and only 148 pounds. Those stats make him sound like a diehard distance runner or a chain smoker.

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