Wheat "debate" on CBC

"Many Canadians plan warm buns, stuffing and pie for their Thanksgiving meals tonight. But I'll speak with a cardiologist who thinks we have no reason to be thankful for any food that contains wheat. William Davis says our daily bread is making us fat and sick."

That's the introduction to my recent interview and debate on CBC, the Canadian public radio system, aired on the Canadian Thanksgiving. Arguing the other side was Dr. Susan Whiting, an academic nutritionist. (I use the word "arguing" loosely, since she hardly argued the issues, certainly hadn't read the book, but was content to echo the conventional line that whole grains are healthy and cutting out a food group is unhealthy.)

I do have to give credit to the Canadian media, including the CBC, who have been hosting some rough-and-tumble discussions about the entire wheat question despite Canada being a world exporter of wheat. I recently participated in another debate with a PhD nutrition expert from Montreal who, in response to my assertion that the genetically-altered high-yield, semi-dwarf strains have changed the basic composition of wheat, argued that the creation of the 2-foot tall semi-dwarf strain was a convenience created so that farmers could see above their fields--no kidding. I stifled my laugh. (The semi-dwarf variants were actually created to compensate for the heavy seed head that develops with vigorous nitrate fertilization that buckles 4 1/2-foot tall wheat stalk, making harvesting and threshing impossible, a process farmers call "lodging." The 2-foot tall semi-dwarf thick, stocky stalk is strong enough to resist lodging.)

In short, debating the nutrition "experts" on this question has been tantamount to arguing with a school age child on the finer points of quantum physics. There has not yet been any real objection raised on the basic arguments against modern genetically-altered wheat. Modern semi-dwarf wheat is, and remains, an incredibly bad creation of the genetics laboratories of the 1970s. It has no business on the shelves of your grocery store nor on the cupboards in your home.

Carrot Cake

This is among my favorite recipes from the Wheat Belly book. I reproduce it here for those of you who read the Kindle or audio version and therefore didn't get the recipes.

I made this most recently this past weekend. It was gone very quickly, as even the 13-year old gobbled it up.

(I reduced the sour cream in this version from 8 to 6 oz to reduce cooking time. Also, note that anyone trying to avoid dairy can substitute more coconut milk, i.e., the thicker variety, in equivalent quantities.)

Makes 8-10 servings



 

 

 

 

 

 

Ingredients:
Cake:
2 cups carrots, finely grated
1 cup chopped pecans
1 cup coconut flour
1 tablespoon ground flaxseed
2 teaspoons ground cinnamon
1 teaspoon allspice
1 teaspoon nutmeg
1 teaspoon baking powder
2 tablespoons freshly grated orange peel
Sweetener equivalent to ½ cup sugar (e.g., 4 tablespoons Truvia)
½ teaspoon sea salt
4 eggs
1/2 cup butter or coconut oil, melted
2 teaspoons vanilla extract
½ cup coconut milk
6 ounces sour cream

Icing:
8 ounces cream cheese or Neufchâtel cheese, softened
1 teaspoon lemon juice
1 tablespoon Truvía or 1/8 teaspoon stevia extract powder or ¼ cup Splenda

Preheat oven to 325° degrees F. Grate carrots and set aside.

Combine coconut flour, flaxseed, cinnamon, nutmeg, baking powder, orange peel, sweetener, and salt in large bowl and mix by hand.

Put eggs, butter or coconut oil, vanilla coconut milk, and sour cream in mixing bowl; mix by hand. Pour liquid mixture into dry pecan/coconut flour mixture and blend with power mixer until thoroughly mixed. Stir carrots and pecans in by hand with spoon. Pour mixture into greased 9- or 10-inch square cake pan.

Bake for 60 minutes or until toothpick withdraws dry. Allow to cool 30 minutes.

Place Neufchâtel cheese in bowl. Add lemon juice and sweetener and mix thoroughly. Spread on cake.

Why wheat makes you fat

How is it that a blueberry muffin or onion bagel can trigger weight gain? Why do people who exercise, soccer Moms, and other everyday people who cut their fat and eat more "healthy whole grains" get fatter and fatter? And why weight gain specifically in the abdomen, the deep visceral fat that I call a "wheat belly"?

There are several fairly straightforward ways that wheat in all its varied forms--whole wheat bread, white bread, multigrain bread, sprouted bread, sourdough bread, pasta, noodles, bagels, ciabatta, pizza, etc. etc.--lead to substantial weight gain:

High glucose and high insulin--This effect is not unique to wheat, but shared with other high-glycemic index foods (yes: whole wheat has a very high-glycemic index) like cornstarch and rice starch (yes, the stuff used to make gluten-free foods). The high-glycemic index means high blood glucose triggers high blood insulin. This occurs in 90- to 120-minute cycles. The high insulin that inevitably accompanies high blood sugar, over time and occurring repeatedly, induces insulin resistance in the tissues of the body. Insulin resistance causes fat accumulation, specifically in abdominal visceral fat, as well as diabetes and pre-diabetes. The more visceral fat you accumulate, the worse insulin resistance becomes; thus the vicious cycle ensues.

Cycles of satiety and hunger--The 90- to 120-minute glucose/insulin cycle is concluded with a precipitous drop in blood sugar. This is the foggy, irritable, hungry hypoglycemia that occurs 2 hours after your breakfast cereal or English muffin. The hypoglyemia is remedied with another dose of carbohydrate, starting the cycle over again . . . and again, and again, and again.

Gliadin proteins--The gliadin proteins unique to wheat, now increased in quantity and altered in amino acid structure from their non-genetically-altered predecessors, act as appetite stimulants. This is because gliadins are degraded to exorphins, morphine-like polypeptides that enter the brain. Exorphins can be blocked by opiate-blocking drugs like naltrexone. A drug company has filed an application with the FDA for a weight loss indication for naltrexone based on their clinical studies demonstrating 22 pounds weight loss after 6 months treatment. Overweight people given an opiate blocker reduce calorie intake 400 calories per day. But why? There's only one food that yields substantial quantities of opiate-like compounds in the bloodstream and brain: wheat gliadin.

Leptin resistance--Though the data are preliminary, the lectin in wheat, wheat germ agglutinin, has the potential to block the leptin receptor. Leptin resistance is increasingly looking like a fundamental reason why people struggle to lose weight. This might explain why eliminating, say, 500 calories of wheat consumption per day yields 3500 calories of weight loss.

And, as in many things wheat, the whole is greater than the sum of the parts. Despite all we know about this re-engineered thing called wheat, eliminating it yields health benefits, including weight loss, that seem to be larger than what you'd predict with knowledge of all its nasty little individual pieces.

Just who is "Real Facts 2000"?

This is an example of what seems to be developing over at Amazon.com, posted as a "book review":

The author has no credentials, no credibility, just a small cult of terribly misinformed followers. Don't be fooled by the high volume screech against wheat and grains. Allegations of "secret ingredients in wheat" to make you eat more, or comparisons to cigerettes. Seriously?! For over 8000 years wheat has sustained and grown human kind, oh and it tastes good when mixed with a little water and yeast. Every nutritionist and serious medical professional will tell you that bread is the most economical and safe source of essential nutrients. In fact, bread is handed out in natural disasters because it sustains life without food safety issues or requiring refrigeration. And now, suddenly it will kill you. Comical! This book is such a bone headed, misinformed way to just scare people into not eating.

As for secret ingredients, humm, apparently the author is ignorant of the food laws that regulate everything that goes into food and on food labels. Unlike some enforcement agencies, the FDA has some serious teeth behind its enforcement. As for frankenwheat, again seriously?! Wheat, due to its ubiquitous presence in the world is treated as sacrosant from any GMO research or development.

If you need real, science based information on healthy eating, check out [...] and leave this book and its cult in the compound.


If you recognize the wording and tone, you will readily recognize the footprints of the Wheat Lobby here. "Terribly misinformed followers"? . . . Hmmm. "Food laws"? I didn't realize that eating more "healthy whole grains" was a . . . law?

Make no mistake: There are people and organizations who have a heavy stake in your continued consumption of the equivalent of 300 loaves of bread per year. There are people and organizations (read: pharmaceutical industry) who have a big stake on the "payoff" of your continued consumption of "healthy whole grains."

This is not a book review; this is part of a concerted, organized campaign to discredit a message that needs to be heard.

Anybody from the media listening?

Almonds are the new wheat

Once you eliminate this genetically-altered Frankengrain called modern wheat, the diet should center around vegetables, nuts, healthy oils like olive and coconut, fish, meats, cheese, olives, avocados and other real whole foods. This is, in fact, the diet that I have advocated in my heart disease prevention practice, as well as my online program for prevention and reversal of heart disease.

But what if you'd like a piece of cheesecake or a nice slice of dessert bread---but you don't want to gain two pounds, spend 48 hours in the bathroom suffering with diarrhea and cramps, 3 weeks of joint pains and leg swelling, wade through mental "fog," anxiety, and rage just because you had that momentary indulgence---as you would with wheat?

That's why I've been focusing on recipes that allow you to have something familiar, e.g., chocolate coconut bread or biscotti, but using ingredients that will not generate the metabolic contortions triggered by wheat.

On perusing these recipes, you will notice that there are recurring ingredient themes. Many of the same ingredients pop up time and again. Among the most frequent, versatile, user-friendly, and tasty: Almonds.

You can use almonds as ground whole almonds, ground blanched almonds for a finer texture, ground roasted almonds, almond butter (though, for maximum health benefits, I prefer the ground whole almonds). Ground almonds allow you to recreate muffins, breads, scones, pizza crust, pie crust, biscotti, and cookies with health benefits that exceed that of whole wheat---but with none of the downside: no weight gain, no high blood sugar, no triggering of small LDL particles (#1 cause of heart disease in the U.S.), no accumulation of visceral fat, no appetite stimulation.

In short, you just have your chocolate almond biscotti or mocha cupcake and enjoy it, no health price to pay. So I call almonds the new wheat, except better.

Being regular is dangerous to your health

No, I'm not referring to your daily morning ritual in the bathroom. I'm talking about heart rate.

Counterintuitively, a perfectly regular heart rate is a marker of poor health. People with perfect regularity of heart rate have more heart attacks, for instance.

Regularity of heart rate occurs more commonly in people with hypertension and other metabolic derangements, and it signals increased risk for both heart attack and death. A perfectly regular heart rate, i.e., no variation in the time interval from beat to beat, suggests that the parasympathetic nervous system, the component of automatic ("autonomic") nervous system control that is associated with the relaxation response, feelings of well-being, quiet, and relaxation, is weak. It also means that the opposing sympathetic nervous sytem that regulates the "fight or flight," adrenaline-like response is allowed to be dominant. Dominance of the sympathetic over the parasympathetic system generates regularity of heart rate. Heart rate also tends to be faster, e.g., 85 beats per minutes rather than 55 or 60 beats per minute. So perfect regularity, as well as increased rate, is undesirable.

What we want is irregularity of heart rate. But not irregularity that occurs chaotically with no rhyme or reason. More precisely, we want variability in heart rate. And we want variability to occur in synchrony with breathing, i.e., the respiratory cycle.

The ideal response is:

1) increase in heart rate with inspiration

2) decrease in heart rate with expiration.

Heart rate in healthy people typically varies 15-20 beats per minute within the respiratory cycle, e.g., 60 bpm at end-exhalation, 80 bpm at end-inspiration.

Restoration of increased heart rate variability is associated with reduced blood pressure, reduced blood sugars (HbA1c), reduced inflammatory markers and cortisol (associated with stress), even an increase in DHEA levels. Feelings of well-being and calm also develop.

Among the strategies to consider to restore heightened heart rate variability and slowed heart rate include:

--Omega-3 fatty acid supplementation
--Exercise
--Weight loss
--Deep breathing exercises
--Meditation, prayer, and biofeedback

For our Track Your Plaque purposes, we are folding in the HeartMath strategies, i.e., use of a heart rate monitor that calculates heart rate variability in the context of respiratory cycle. If you've not already done so, take a look at the two Special Reports devoted to this topic on the Track Your Plaque website.

You mean weight loss is hazardous to your health?

In my last Heart Scan Blog post, What is this wacky thing called weight loss?, I discussed how weight loss is associated with distortions in cholesterol and blood sugar values that can be very confusing, often leading your doctor to wrongly and unnecessarily prescribe drugs--since he/she likely rarely sees weight loss.

Blog reader, Donald K., posted his enlightening story:

I experienced this very thing.

After losing serious weight from the eliminating wheat, processed, and sugary foods (1 year in total) I lost 130 pounds. When I was nearly finished I went to see my doctor. He wanted to put me on statins. I explained to him how the data does not support application to me (no evidence of heart disease) and I got the mantra about standards of practice, etc, etc. I held my ground and decided I am much happier eating dairy, eggs, grass fed beef, wild caught fish, and as much raw foods (nuts, veggies, fruits) as my body desires to treat my health parameters.

Maintaining weight, it is easy. My BMI (23 down from 40) has remained constant for a few months now. You are right: metabolic processes definitely change. I no longer have sensations of glucose fluctuations or an uncontrolled appetite. I can only imagine the improved hormone regulation and metabolic communication going on inside my body.

The symptoms from obesity, all gone. Goodbye sleep apnea, hypertension, hemorrhoids, arrhythmias, gastroinestinal disruptions, smelly body, chaffing thighs, and others not mentioned. The positive effects are just as dramatic, but I don’t want to ramble on.

Weight loss? What is it? Getting your life back!


Brace yourself: If you are following the nutrition advice posted here and in the Track Your Plaque program, or the discussion I've initiated in Wheat Belly, then you may find yourself in the very same health predicament as Donald. Arm yourself to protect yourself against the drug-wielding ways of doctors. No, weight loss to achieve ideal weight is definitely not bad for health. But your doctor's misinterpretation of its effects can be!

What is this wacky thing called "weight loss"?

I've discussed this before, but it has proven such an (encouragingly!) frequent issue that I thought it was worth discussing once again.

What happens when you lose weight?

The process of weight loss is characterized by multiple shifts in metabolic patterns that can be confusing. To the uninitiated eye, weight loss can look like a disastrous distortion in metabolism. The naive doctor on seeing your lab values, for instance, might insist you take a statin drug, a fibrate like Tricor (to reduce triglycerides or increase HDL), or simply berate you for your bad health habits--when it's actually a good thing you've accomplished.

So when you lose weight, say, 30 pounds in 3 months, what have you accomplished?

Energy stored as fat, especially from visceral fat stores, is mobilized into the bloodstream. It floods the bloodstream as fatty acids and triglycerides. These fatty acids and triglycerides don't occur in isolation, but interact with other particles and metabolic patterns. The resulting blood patterns include:

--Increased triglycerides--An increase in triglycerides, for instance, from 90 mg/dl to 200 mg/dl in the midst of weight loss is common.

--Reduced HDL--The flood of triglycerides leads to increased degradation of HDL, thus a drop. A drop in HDL from, say, 40 mg/dl to 27 mg/dl--very frightening to people--is exceptionally common.

--Increased blood sugar--The flood of fatty acids and triglycerides results in insulin resistance, leading to higher blood sugars. It is not uncommon for someone with pre-diabetes to develop diabetic-range blood sugars, or a non-diabetic to show pre-diabetic blood sugars.

--Increased small LDL particles--Though small LDL is highly variable during weight loss. When it does happen, it's probably from the interaction of VLDL (triglycerides) with LDL particles and the reaction that overloads LDL particles with triglycerides and conversion to small LDL particles.

So why don't doctors often recognize these patterns when a patient loses weight? Because they rarely see it. Most of my colleagues are accustomed to having patients come back with weight gain, getting heavier and heavier each time. Lose weight? Impossible! So they just don't recognize weight loss effects when they see it. As followers of The Heart Scan Blog know, a frequent conversation around here is "Am I too skinny?" or "How do I stop losing weight?"

The solution: Be patient. Be patient and wait about two months after a weight plateau has been achieved. That's when the numbers "settle down" and you see marked drops in triglycerides, increases in HDL, drops in blood sugar, reductions in small LDL.

As with many things, it's all about timing.

Why small LDL particles are the #1 cause of heart disease in the US

Ask your doctor: What is the #1 cause of heart disease in the US?

Let's put aside smoking, since it is an eminently modifiable risk and none of those crazies read this blog anyway. What will your doctor say? Most like he or she will respond:

High cholesterol or high LDL cholesterol

Too much saturated fat

Obesity

Pfizer, Merck, AstraZeneca and their kind would be overjoyed to know that they can add your doctor to their eager following.

I'd tell you something different. I would tell you that small LDL particles are, by far and away, the #1 cause for heart disease. I base this claim on several observations:

--Having run over 10,000 lipoprotein panels (mostly NMR) over the past 15 years, it is a rare person who does not have a moderate, if not severe, excess of small LDL particles. 50%, 70%, even 90% or more small LDL particles are not rare. Over the course of a year, the only people who show no small LDL particles are slender, athletic, pre-menopausal females.

--In studies in which lipoproteins have been quantified in people with coronary disease, small LDL particles dominate, just as they do in my office. Here's a 2006 review.

--Small LDL is largely the province of people who consume carbohydrates, such as the American population instructed to "cut fat and eat more healthy whole grains." Conventional diet advice has therefore triggered an expllosion in small LDL particles.

--When fasting triglycerides exceed 60 mg/dl, small LDL particles increase as a proportion of total LDL particles. This includes the majority of the US population. (This ignores postprandial, or after-eating, triglycerides, which also contribute to small LDL formation.)

If you were to read the data, however, you might conclude that small LDL affects a minority of people. This is because in most studies small LDL categorize it as either "pattern B," meaning exceeding some arbitrary threshold of percentage of small LDL particles, versus "pattern A," meaning falling below that same arbitrary threshold.

Problem: There is no consensus on what percentage of small LDL particles should mark the cutoff between pattern A vs. pattern B. In many studies, for instance, people with 50% small LDL particles are called "pattern A."

If, instead, we were to set the bar lower to identify this highly atherogenic (atherosclerotic plaque-causing) particle at, say, 20-30% of total, then the number or percentage of people with "pattern B" small LDL particles would go much higher.

I see this play out in my office and in the online program, Track Your Plaque, every day: At the start eating a low-fat, grain-filled diet with lots of visceral fat ("wheat belly") to start, they add back fat and cut out all wheat and limit carbohydrates. Small LDL particles plummet

Even moore from Jimmy Moore

The ubiquitous and irrepressible Jimmy Moore posted even more commentary about the Wheat Belly phenomenon here, what he calls "The Wheat Belly Bonanza."

Is low-carb really, at its core, little more than elimination of wheat? Sure, corn, rice, and sugar exert deleterious effects. But the dominant effect--by far--is the elimination of wheat. So is the low-carb movement really, at its core, a wheat-elimination movement?

Food (non-wheat-containing, of course) for thought.
When MIGHT statins be helpful?

When MIGHT statins be helpful?

I spend a lot of my day bashing statin drugs and helping people get rid of them.

But are there instances in which statin drugs do indeed provide real advantage? If someone follows the diet I've articulated in these posts and in the Track Your Plaque program, supplements omega-3 fatty acids and vitamin D, normalizes thyroid measures, and identifies and corrects hidden genetic sources of cardiovascular risk (e.g., Lp(a)), then are there any people who obtain incremental benefit from use of a statin drug?

I believe there are some groups of people who do indeed do better with statin drugs. These include:

Apoprotein E4 homozygotes

Apoprotein E2 homozygotes

Familial combined hyperlipidemia (apoprotein B overproduction and/or defective degradation)

Cholesteryl ester transfer protein homozygotes (though occasionally manageable strictly with diet)

Familial heterozygous hypercholesterolemia, familial homozygous hypercholesterolemia

Other rare variants, e.g., apo B and C variants

The vast majority of people now taking statin drugs do NOT have the above genetic diagnoses. The majority either have increased LDL from the absurd "cut your fat, eat more healthy whole grains" diet that introduces grotesque distortions into metabolism (like skyrocketing apo B/VLDL and small LDL particles) or have misleading calculated LDL cholesterol values (since conventional LDL is calculated, not measured).

As time passes, we are witnessing more and more people slow, stop, or reverse coronary plaque using no statin drugs.

Like antibiotics and other drugs, there may be an appropriate time and situation in which they are helpful, but not for every sneeze, runny nose, or chill. Same with statin drugs: There may be an occasional person who, for genetically-determined reasons, is unable to, for example, clear postprandial (after-eating) lipoproteins from the bloodstream and thereby develops coronary atherosclerotic plaque and heart attack at age 40. But these people are the exception.

Comments (17) -

  • Might-o'chondri-AL

    4/8/2011 12:21:11 AM |

    I don't know how individuals with mis-sense SNP for gluco-kinase regulatory protein (ex: GCKR rs780094) fit into the pattern. They get more liver steatosis (fat build up) with attendant elevated LDL and triglycerides, despite less fasting glucose and less fasting insulin numbers; while their 2 hour blood glucose runs high (GCK gene is very determinate of 2 hour glucose levels), showing down-regulation of the homeostatic model for Beta cell function (HOMA-B).

    Normally GCKR regulates triglycerides and determines persons glycemic traits by governing how glucose is stored and how it is dispersed. GCKR also geneticly regulates the availablility of substrate used for de-novo lipo-genesis.

    Gene SNP of protein phosphatase 1regulatory (inhibitor) subunit 3 B (PP1R3B rs4240624) manifests increased liver steatosis  and both elevated LDL and elevated HDL; with low fasting glucose. PPP1R3B codes for controling protein and modulates the break down of glycogen (storage glucose moleccule).

    Together PPP1R3B and GCKR are integral to blood sugar dynamics and the levels of lipids in circulation.

    If Doc's regimen counter-balances individual missense genetic workings, like those above, then that is impressive corrrection achieved through intervention . I presume for people with liver steatosis missense mutations (ie:  SNPs like above) elevated LDL treatment using statins would be bad for their liver.

  • Dr. John

    4/8/2011 1:10:14 AM |

    Statins might be helpful if you have bacterial pneumonia:
    http://www.bmj.com/content/342/bmj.d1907.extract?sid=f762e55c-1a0b-4ef3-81c4-f31cc472a372

    That's because the rapidly growing pneumococcal bacteria are very susceptible to HMG-CoA reductase inhibitors (statins). The bacteria have similar cholesterol compounds (hopanoids) in their membranes, essential for their membrane function. With the statins blocking the hopanoids, they die....very quickly.

    All bacteria have a mevalonate pathway.  The HMG-CoA reductase enzyme is inhibited in bacteria and are VERY toxic to bacteria. So thus, you have a "statin-benefit" because it kills the bacteria, before it kills or injures the patient.

    Statins can essentially inhibit biological life forms.
    Dr. John

  • Dr. William Davis

    4/8/2011 1:11:01 AM |

    HI, Might--

    As usual, you've come out of left field with a totally unexpected issue!

    I'm not sure how this genetic variant fits into this argument. It is, to my knowledge, a very rare diagnosis.

  • Might-o'chondri-AL

    4/8/2011 6:40:15 PM |

    I don't envy Doc trying to sort out who needs what treatment. Genetic high cholesterol entails over 50 amino acid variations out the jumble of 692 amino acids assembled into relevant complexes.

    Pro-protein convertase subtilisin/kexin-9 (PCSK9)is involved in familiar hyper-cholestemia. Those who make too much PCSK9 (in the liver and small intestine) rapidly degrade their cholesterol receptors and can't pluck much LDL out of circulation; plasma cholesterol rises.

    Should one's genetics foster making too little PCSK9, then cholesterol receptors don't degrade. This promptly shunts cholesterol into the liver lysosome (an organelle inside a cell)for break down; thus they  measure low cholesterol in the blood.

    I speculate Doc's diet, in "normal" genetic people up-regulates cholesterol reception. Which means his program has the epigenetic effect (from diet dynamics) on "normal" liver/small intestine genes in a way that less PCSK9 is expressed

    The caucasian anglo-saxon PCSK9 D374Y mutation causes 4 times the normal cholesterol in patients. Their risk factor for pre-mature death is 10 years earlier than even more benign PCSK9 mutations; so Detective Doc Davis is willing to prescribe statins for people like them.

  • Anonymous

    4/9/2011 2:59:55 AM |

    I might be one of these poor souls.

    Eating a strict diet, one Dr Davis would be very proud of... I'm lean as can be, feel great, but my cholesterol shot through roof (while HDL dropped).    

    Frown

  • Might-o'chondri-AL

    4/9/2011 4:53:48 AM |

    Hi Annon.,
    Internet self-diagnosing shouldn't replace a good medical consultant. My comments are not qualified medical assesments; am a layman.  

    My favorite cousin has had her cholesterol testing well over 300for several decades, and is now in her late 70s. Like Doc chided me earlier, there are "genetic variant" being "very rare diagnosis."

  • Lucy

    4/9/2011 11:47:29 AM |

    What do you think about KIF6?   I was tested and found to be a non-carrier, and I was subsequently told that statins would likely not benefit me as much as diet/lifestyle changes (I'm ApoE 3/4 as well).  Does that also mean that niacin would not help?

  • Anonymous

    4/9/2011 12:52:56 PM |

    To say the least, I am very disappointed in Dr. Davis' stance regarding ApoE 4 & statins. There is abundant evidence suggesting statins are counterproductive to brain health, which is much more pronounced in Apo E4's who are already at high risk for alzheimers disease. It isn't only about lipids, there is a larger picture to consider. The brain requires cholesterol.  Also, high cholesterol levels are associated with longevity in the elderly.

  • Might-o'chondri-AL

    4/9/2011 7:44:42 PM |

    Alzheimers and the relationship of ApoE4 is different than other ApoE isoforms (like ApoE 2 & 3). In normal people ApoE is integral to clearing amyloid Beta from the brain; it forms a conjugate (ApoE/AmyloidB)that is moved out across the brain blood barrier by LRP-1 (lipo-protein related protein 1).

    ApoE4 is acted upon (cleaved) in brain neurons, yielding rump fragments with unique Carbon- terminals; and,  ApoE4 degrades easier than ApoE 2 &/or 3. These ApoE4 fragments, when in a brain cell's cytosol, influence that cell's mitochondria hydro-phobic pattern of lipid binding.

    The ApoE4 fragment properties  do 2 unwanted things to the brain cell mitochondria. It decreases the mitochondria ability to perform tasks involved in glycolysis (glucose energy). And is antagonistic to PPAR gamma; PPAR gamma is what would otherwise promote adequate mitochondria bio-genesis.

    ALzheimer lesions show higher amounts when measured in individuals with concurrent Type II diabetes and the ApoE4 isoform. The ratio of insulin in the cerebro-spinal fluid to the amount of insulin in the blood also shows a difference depending on the specific ApoE geno-type.

    Alzheimer brains are using less glucose; patients show less receptors for insulin-like growth factor and insulin, as well as less insulin degrading enzymes. It is postulated that depending on the individual's ApoE variation there is a different amyloid Beta response to brain insulin.

    Normally one goes from glucose intolerance to hyperglycemia and then elevated insulin circulating as become diabetic. Yet experiments show that giving insulin improves diabetic neuro-pathy in the brain; it seems to be a way peripheral insulin resistance causes different tissues to respond.

    In Alzheimer experiments with supplemental insulin (nasal, etc.)administration cognitive function improved. This response was more significant in those with the ApoE4 allele (compared to other ApoE types with Alzheimers, who also improved cognition ).

    So, the Alzheimer enigma seems to involve energy format dynamics for ApoE isoforms more than specific levels of cholesterol. This is not a comment on ApoE homo-zygote genes relationship to cardio-vascular risk factors, or brain lipid metabolism.

  • homertobias

    4/11/2011 3:36:34 PM |

    Mito
    You sound like Suzanne Craft.  I like her work.

  • Medicomp INC.

    4/12/2011 4:06:52 PM |

    You make an excellent point here:

    ...eat more healthy whole grains" diet that introduces grotesque distortions into metabolism

    We are encouraged by transient sources that this is almost always the best alternative for other fattening foods, yet people never really delve deep into the cons of this transition either.  It truly does take dedication to be well-informed about the dietary changes you make in your lifestyle.

  • Anne

    9/18/2011 5:58:38 PM |

    I had a body scan a few years ago, and my plaque count was 1050, when they told me that 150 was considered high, I thought  I would implode at any moment, I went to a lot of different cardiologists and had all kinds of tests and they said to exercise and not  worry about the plaque. One Dr. put me on lipitor and 3 days later I could hardly walk from the muscle pain, he told me to stop taking it and I tried niacin and red rice with the same results. I don't know how to reduce the plaque, the Dr's all said it was hereditary . I am open to any advice.

  • Dr. William Davis

    9/20/2011 12:43:37 PM |

    Hi, Anne--

    Note that this is the blog that accompanies the Track Your Plaque program that focuses on just this issue. It means 1) identify all causes of plaque, then 2) correct them, preferably using natural means.

  • JK

    10/30/2011 4:52:34 PM |

    Dr. Davis,
    I don't know if you have already addressed this topic in prior posts but allow me to suggest that in lieu of consuming statin drugs, even for the aforementioned outliers, it is possible to achieve reduced LDL cholesterol and increased HDL cholesterol by supplementing with magnesium.
    (All the ensuing statements below I humbly attribute to Mildred S. Seelig and Andrea Rosanoff, "The Magnesium Factor," pages 139-147.)
    1. Statins (Lipitor, Zocor, Baycol, Mevacor, etc.) are designed to lower cholesterol by inhibiting HMG-CoA reductase, which is the enzyme responsible for the synthesis of cholesterol.
    2. These drugs when studied, not only lower cholesterol, but also reduce total mortality, cardiac mortality, the total incidence of heart attacks, angina, and other non-fatal cardiac events. (p.140.)
    3. They also made the blood platelets less sticky, they slowed the progression of plaques and stabilized them, and they reduced inflammation in the blood vessel tissue. (ibid.)
    All these results, and more, Seelig further informs the reader, are a result of reduced mevalonate in the cells, which is the direct result of an inhibited HMG-CoA reductase, which is the enzyme that statins are designed to inhibit.
    Now stay with me for a second because here is where it gets interesting.
    4. Magnesium is a natural inhibitor of HMG-CoA reductase. Here magnesium and statins are comparable (p. 141.)
    5. Magnesium also acts on two enzymes, phosphatase reductase and phosphohydrolase which reactivate HMG-CoA reductase. By its effects on these enzymes, which contrast one another, magnesium can either stop cholesterol formation or allow it to continue depending on the body's needs.
    6. Magnesium also activates another enzyme, lecithin cholesterol acyltransferase (LCAT) which, through this action, converts LDL cholesterol to HDL cholesterol -- increasing HDL and reducing LDL.  (Statins cannot do this.)
    In the interest of brevity, I'll conclude by saying that whereas statins are known to reduce cholesterol and perhaps achieve other cardiovascular benefits, this is due in large part to their suppression of mevalonate, brought about by their inhibition of HMG-CoA reductase.
    In contrast, magnesium not only inhibits HMG-CoA reductase, meaning that it would achieve the same results as statins in "1, 2, and 3 above," but it also converts LDL cholesterol to HDL cholesterol, achieved by its activation of LCAT, which is something that statins do less consistently.
    Further, instead of poisoning HMG-CoA reductase as statins do, magnesium inhibits it in ways that can be reactivated by other (magnesium dependent) enzymes so that the body can naturally make the mevalonate and cholesterol it needs.
    This is important because vitamin D is synthesized from cholesterol (when using the sun's rays), and cholesterol is also the precursor to testosterone, estrogen, and other steroids.
    So I encourage you to consider using Magnesium for those Apo-B cases that cannot be addressed by carbohydrate restricted diets.

  • JK

    10/30/2011 4:58:10 PM |

    Sorry, meant to say Apo-E cases.

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