Texas today, tomorrow . . . the world?

10. March 2009 William Davis (0)
Texas state representative, Rene Oliveira, has introduced legislation that mandates heart scans for adults in the state of Texas.

Rep. Oliveira

A press release from the SHAPE Society ( Society for Heart Attack Prevention and Eradication) reads:

Assessment of heart attack risk on the basis of traditional risk factors alone such as high cholesterol and high blood pressure and so forth, while useful, misses many who are at high risk and also incorrectly flags some for high risk who are in fact at very low risk of near term heart attack; on the other hand detection of atherosclerosis by non-invasive imaging, as suggested by the SHAPE group, accurately identifies plaque and improves the ability to identify at-risk individuals who could benefit from aggressive preventive intervention while sparing low-risk subjects from unnecessary aggressive medical therapy," said Dr. P.K. Shah, Director of Cardiology at Cedars Sinai Heart Institute in Los Angeles, a leading member of the SHAPE Task Force who is also an active member of the American Heart Association. "Sadly, these vulnerable patients go undetected until struck by a heart attack, because insurance companies don't cover the newer heart attack screening imaging tests."


Rep. Oliveira, whose coronary disease was first uncovered by a heart scan and prompted a bypass operation, states:

"It is about time that we cover preventive screening for the number one killer in Texas, and take action to reduce healthcare costs through preventive healthcare. Right now, we are extending the lives of those who can afford the procedure while hundreds of thousands of Texans with hidden heart disease go undetected because of antiquated thinking. The time has come for this change."


Is this what we've come to? Since practicing physicians are either so entranced by the drug and procedural solutions to heart disease, do we need to resort to heart scan by legislation?

It does indeed appear that we've come to this point. Should this trend catch on, it will surely mean an upfront increase in healthcare costs to cover the expense of heart scans. But in the long run, it will mean reduction in healthcare costs--dramatic reduction--if heart scans prompt effective preventive action.
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"I don't know what I'm doing here"

"I don't know what I'm doing here"

25. October 2006 William Davis (0)
Jim came to the office at the prompting of his wife.

At age 52, Jim was semi-retired, having to work only a few hours a week to maintain his business. He'd had a high cholesterol identified about 10 years earlier and had been taking one or another statin drug ever since.

However, Jim's wife was a pretty savvy girl and understood the inadequacies of the conventional approach to heart disease prevention. Nonetheless, when Jim came in, he declared, "I feel great. I don't know what I'm doing here!"

I persuaded Jim to undergo a heart scan. His score: 2211, in the 99th percentile (the worst 1% for men in his age group). However, it was worse than that. Any score above 1000 carries a heart attack risk of 25% per year unless prevention issues are fully addressed.

Indeed, Jim proved to have far more than a high LDL cholesterol. Among the patterns uncovered with his lipoprotein analysis were small LDL, the postprandial (after-eating) abnormality of intermediate-density lipoprotein (IDL), and high triglycerides and VLDL. All would require correction if Jim is to hope to gain control of his extensive coronary plaque.

The message: Trying to discern risk for heart disease from cholesterol is complete folly. This man was going to die or have an urgent major heart procedure within the next year or two, all while taking his statin drug.

Discard the silly notion that cholesterol tells you everything you need to know about heart attack risk. It does not. It helps a little but leaves vast voids in risk determination. Fill those gaps with a heart scan, plain and simple.
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Kick inflammation in the butt

Kick inflammation in the butt

25. June 2010 William Davis (0)
C-reactive protein, or CRP, is a protein produced by the liver in response to inflammatory signals its receives. Thus, CRP has emerged as a popular measure to gauge the underlying inflammatory status of your body. Higher CRP levels (e.g., 3.0 mg/L or greater) are associated with increased risk of heart attack and other cardiovascular events.

The drug cartel have jumped on this with the assistance of Harvard cardiologist, Dr. Paul Ridker. Most physicians now regard increased CRP as a mandate to institute statin therapy, preferably at high doses based on such studies as The JUPITER Trial, in which rosuvastatin (Crestor), 20 mg per day, reduced CRP 37%.

I see this differently. Two strategies drop CRP dramatically, nearly to zero with rare exception: Vitamin D restoration and wheat elimination. Not 37%, but something close to 100%.

Yes, I know it sounds wacky. But it works almost without fail, provided the rest of your life is conducted in reasonably healthy fashion, i.e., you don't live on Coca Cola, weigh 80 lbs over ideal weight, and smoke.

How can something so easily reduced like CRP mean you "need" medication? Easy: Increased CRP means there are fundamental deficiencies and/or inflammation provoking foods in your diet. Correct neither and there is an apparent benefit to taking a statin drug.

Why not just correct the underlying causes?
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When MIGHT statins be helpful?

When MIGHT statins be helpful?

7. April 2011 William Davis (17)
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.
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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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Carbohydrate sins of the past

Carbohydrate sins of the past

17. February 2010 William Davis (15)
Fifty years ago, diabetes was a relatively uncommon disease. Today, the latest estimates are that 50% of Americans are now diabetic or pre-diabetic.

There are some obvious explanations: excess weight, inactivity, the proliferation of fructose in our diets. It is also my firm belief that the diets advocated by official agencies, like the USDA, the American Heart Association, the American Dietetic Association, and the American Diabetes Association, have also contributed with their advice to eat more “healthy whole grains.”

When I was a kid, I ate Lucky Charms® or Cocoa Puffs® for breakfast, carried Hoho’s® and Scooter Pies® in my lunchbox, along with a peanut butter sandwich on white bread. We ate TV dinners, biscuits, instant mashed potatoes for dinner. Back then, it was a matter of novelty, convenience, and, yes, taste.

What did we do to our pancreases eating such insulin-stimulating foods through childhood, teenage years, and into early adulthood? Did our eating habits as children and young adults create diabetes many years later? Could sugary breakfast cereals, snacks, and candy in virtually unlimited quantities have impaired our pancreas’ ability to produce insulin, leading to pre-diabetes and diabetes many years later?

A phenomenon called glucose toxicity underlies the development of diabetes and pre-diabetes. Glucose toxicity refers to the damaging effect that high blood sugars (glucose) have on the delicate beta cells of the pancreas, the cells that produce insulin. This damage isirreversible: once it occurs, it cannot be undone, and the beta cells stop producing insulin and die. The destructive effect of high glucose levels on pancreatic beta cells likely occurs through oxidative damage, with injury from toxic oxidative compounds like superoxide anion and peroxide. The pancreas is uniquely ill-equipped to resist oxidative injury, lacking little more than rudimentary anti-oxidative protection mechanisms.

Glucose toxicity that occurs over many years eventually leaves you with a pancreas that retains only 50% or less of its original insulin producing capacity. That’s when diabetes develops, when impaired pancreatic insulin production can no longer keep up with the demands put on it.

(Interesting but unanswered question: If oxidative injury leads to beta cell dysfunction and destruction, can antioxidants prevent such injury? Studies in cell preparations and animals suggest that anti-oxidative agents, such as astaxanthin and acetylcysteine, may block beta cell oxidative injury. However, no human studies have yet been performed. This may prove to be a fascinating area for future.)

Now that 50% of American have diabetes or pre-diabetes, how much should we blame on eating habits when we were younger? I would wager that eating habits of youth play a large part in determining potential for diabetes or pre-diabetes as an adult.

The lesson: Don’t allow children to repeat our mistakes. Letting them indulge in a lifestyle of soft drinks, candy, pretzels, and other processed junk carbohydrates has the potential to cause diabetes 20 or 30 years later, shortening their life by 10 years. Kids are not impervious to the effects of high sugar, including the cumulative damaging effects of glucose toxicity.
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Comments (15) -

  • Matt Stone

    2/18/2010 3:13:57 AM |

    The government advice to "eat more healthy whole grains" is not off-base.  But that's not what Americans did.  Instead they ate more fructose and replaced saturated fats with more polyunsaturated fats.  This is totally fundamentally different than eating a low-fat, high-carbohydrate diet like that of the rural Zulu tribe studied by T.L. Cleave or the Africans studied by Denis Burkitt and Hugh Trowell that were diabetes and obesity-free.  

    Americans are still not even coming close to the grain consumption of a century ago, when such diseases were exceedingly rare.

  • Mat

    2/18/2010 5:38:50 AM |

    This video is very good:

    "Vitamin D and Diabetes-Can We Prevent it?"

    http://www.youtube.com/watch?v=wTtmvMvgfl0

  • TedHutchinson

    2/18/2010 9:54:56 AM |

    At this link you'll find the slides of a short presentation on
    The Influence of high vs. low sugar cereal on children's breakfast consumption.
    There are some surprising findings.

    I found it at Cerealfacts.org website

    The situation in the UK is much the same. The breakfast cereals most likely to find at discounted prices are those with the most sugar.

    It's  often the case the choice of cereal going into the trolley is made by the child rather than the parent. There should be more restrictions on the promotion of pre-sweetened cereals to kids.

  • Anonymous

    2/18/2010 12:36:43 PM |

    In my early 60s I notice that I don't get much "kick" out of sugary foods as I might have earlier.  I've gotten to the point where I can't believe the amount of sugar in say cookies or ice cream...which I no longer buy.  

    I do now take several phyto-extracts...pomegranate...blueberry...cocoa...resveratrol...green tea...grape seed...etc.

    Pomegranate at least has been shown to moderate insulin response and maybe reverse atherosclerosis.

    http://www.lef.org/LEFCMS/aspx/PrintVersionMagic.aspx?CmsID=114814

  • Dr.A

    2/18/2010 2:04:35 PM |

    Great post!
    I've just blogged about my eating history too...  years of low-fat, high starch, high fruit eating led me to the brink of diabetes. I'm amazed I survived childhood!

  • SuzyCoQ

    2/18/2010 5:34:51 PM |

    Interesting, but this leaves out neogenesis within the pancreas. Assuming that glucose intake is reduced, wouldn't new beta cells be undamaged and have full functionality? [Unless progenitor cells are also damaged...]

  • Nancy

    2/18/2010 8:15:00 PM |

    Wouldn't this be more along the lines of adult onset type 1 diabetes (insulin dependent)?  It seems like that is growing too but the real swell seems to be in Type 2 diabetes where you produce copious amounts of insulin but your tissues are resistant to it.

  • whatsonthemenu

    2/18/2010 10:28:00 PM |

    "Interesting, but this leaves out neogenesis within the pancreas. Assuming that glucose intake is reduced, wouldn't new beta cells be undamaged and have full functionality? "

    That explains why my obese elderly mom has normal blood sugars even though she has always eaten diet high in simple carbs.

  • DrStrange

    2/19/2010 5:46:28 PM |

    Dr. A, your previous diet was indeed low fat and starch based but there was not much actual, real food in it!  I am missing the connection both here on this thread and in your blog, between people eating manufactured, food like substances that don't have much fat in them and are loaded w/ refined/highly processed starch carbs w/ almost zero fiber or nutrients in them, and the eating of actual whole grains, either fully intact or minimally processed.

  • whatsonthemenu

    2/19/2010 9:43:28 PM |

    "Wouldn't this be more along the lines of adult onset type 1 diabetes (insulin dependent)? It seems like that is growing too but the real swell seems to be in Type 2 diabetes where you produce copious amounts of insulin but your tissues are resistant to it."

    If you haven't already, check out Jenny Ruhr's blog, Diabetes Update, and her related website, Diabetes 101.  Type II is being subdivided according to short and long-term beta cell function and insulin resistance.  Different genes cause different impairments.  Emerging is MODY (mature onset diabetes of the young), or type 1.5.  A defining characteristic is that the ability of the pancreas to secrete insulin declines slowly over time, rather than suddenly as in type I, but it declines no matter what the treatment.

  • Michael Barker

    2/20/2010 5:40:01 AM |

    I am a Ketosis Prone Type 2 diabetic and it isn't necessarily true that glucose toxicity leads to permanent loss of pancreas functioning.

    Typically, we will lose all pancreas secretion and will go DKA, at that point we are essentially type 1's. We need insulin to survive but after 2 to twelve weeks of normal blood sugars we can be taken off insulin and we will have near normal blood sugars.

    Weird, yes, but there are thousands of us out there so this isn't uncommon.

    Narrative Review: Ketosis-Prone Type 2 Diabetes Mellitus
    http://www.annals.org/content/144/5/350.abstract

    My blog has more information, if you are interested.

    We seem to be severely intolerant of carbs so I too wonder what would have been the case, if years ago the carbs were taken out of my diet.

  • Anonymous

    2/22/2010 5:20:40 AM |

    Michael Barker - your blog is fascinating. Thanks for the pointer. Will you be allowing comments?

  • Anonymous

    2/26/2010 9:30:44 PM |

    What a great resource!

  • Nigel Kinbrum

    2/27/2010 3:35:57 PM |

    Matt Stone said...
    "The government advice to "eat more healthy whole grains" is not off-base. But that's not what Americans did." The public were conned. Manufacturers turned whole grains into dust and formed the dust into junk. Because everything that was in the grain was in the junk, they called the junk "whole grain".

  • Anonymous

    10/20/2010 3:35:26 AM |

    Sadly, this is what happened to me. I had glucose problems by age 15, but they told me for years I was fine. There was less information available in those days. I stopped all soda and junk, but it was too late, my fate was sealed. My pancreas and teeth were damaged. Somehow I managed to eat fruit without getting headaches years later, so I thought fruit in moderation was healthy. I though my fatigue was from my mercury fillings, but now I realize some of my fatigue was from fruit sugar. I blame society and my parents, although I forgive my parents. I was fed tons of soda and every type of high glycemic junk food you can imagine.

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