Eat fish three times a day

29. October 2006 William Davis (1)
Patients commonly ask, "Why can't I get vitamin D from food? I drink milk and eat fish."

They're absolutely right: both vitamin D and some oily fish contain vitamin D. However, it's a matter of quantity. An 8 oz. glass of milk contains 100 units of vitamin D (at least it's supposed to; this is not always true). A serving of oily fish like salmon or herring may contain up to 400 units. Thus, if you ate fish three times a day like the Eskimos or the Inuit, you might obtain sufficient vitamin D to prevent the broad and alarming spectrum of phenomena associated with deficiency.

I suspect that most people don't want to eat fish three times a day, nor drink the 20 to 50 glasses of milk per day that would be required to obtain a truly healthy quantity of vitamin D.

The vocal and outspoken Dr. John Cannell of the Vitamin D Council (www.vitamindcouncil.com) has written eloquently on the potential relationship between influenza and vitamin D deficiency. He and his co-authors on a recently published paper point out that the peculiar and unexplained seasonality of influenza corresponds to vitamin D levels. Read his eloquent discussion in Medical News Today at http://www.medicalnewstoday.com/medicalnews.php?newsid=51913.

In the article, Dr. Cannell explains:

"The vitamin D steroid hormone system has always had its origins in the skin, not in the mouth. Until quite recently, when dermatologists and governments began warning us about the dangers of sunlight, humans made enormous quantities of vitamin D where humans have always made it, where naked skin meets the ultraviolet B radiation of sunlight.
We just cannot get adequate amounts of vitamin D from our diet. If we don't expose ourselves to ultraviolet light, we must get vitamin D from dietary supplements...Today, most humans only make about a thousand units of vitamin D a day from sun exposure; many people, such as the elderly or African Americans, make much less than that. How much did humans normally make? A single, twenty-minute, full body exposure to summer sun will trigger the delivery of 20,000 units of vitamin D into the circulation of most people within 48 hours. Twenty thousand units, that's the single most important fact about vitamin D. Compare that to the 100 units you get from a glass of milk, or the several hundred daily units the U.S. government recommend as “Adequate Intake.” It's what we call an “order of magnitude” difference.

"Humans evolved naked in sub-equatorial Africa, where the sun shines directly overhead much of the year and where our species must have obtained tens of thousands of units of vitamin D every day, in spite of our skin developing heavy melanin concentrations (racial pigmentation) for protecting the deeper layers of the skin. Even after humans migrated to temperate latitudes, where our skin rapidly lightened to allow for more rapid vitamin D production, humans worked outdoors. However, in the last three hundred years, we began to work indoors; in the last one hundred years, we began to travel inside cars; in the last several decades, we began to lather on sunblock and consciously avoid sunlight. All of these things lower vitamin D blood levels. The inescapable conclusion is that vitamin D levels in modern humans are not just low - they are aberrantly low."


Like Dr. Cannell, I am absolutely convinced that vitamin D deficiency plays an important role in a number of illnesses, including coronary disease. The more we mind our patients/participants vitamin D status (blood levels of 25-OH-vitamin D3), the more easily we gain control over LDL cholesterol, pre-diabetic patterns, blood pressure, blood sugar, and coronary plaque. In fact, I am becoming rapidly convinced that vitamin D deficiency is an extremely important coronary risk factor.

Because I live in Wisconsin (bbrrrrr!) where seeing the sun is a cause for celebration and sun exposure is possible three months a year, I take 6000 units per day vitamin D. This is the amount necessary to raise my blood levels into the true, physiologic range of 50-70 ng/ml. My wife takes 2000 units per day, and each of my kids takes 1000 units per day, though I believe that my 14-year old son (my size now) should take more. We'll judge by blood levels.

If there is a little-known secret to reducing heart scan scores, vitamin D is that "secret".

To read more from Dr. Cannell or to subscribe to his free and very informative newsletter, go to Vitamin D Council
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Comments (1) -

  • Anonymous

    11/13/2006 10:54:00 PM |

    Cod Liver Oil is an excellent source of vitamin D too - and it's natural, not added like you'll find in low-fat/no-fat milk and dairy - also of note, butter, cream, natural cheese, plain whole yogurt, etc. also contain vitamin D.  Remove the fat, remove the vitamin D - and if it's not fortified to add it back, it's a lost opportunity to get in vitamin D with food.

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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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