Calling all super-duper weight losers!






Have you lost at least 1/2 your weight, e.g., 300 lbs down to 150 lbs? If you have, I have a major national magazine editor looking to talk to you.

If you have gone wheat-free and/or followed the dietary advice offered here in The Heart Scan Blog or through the Track Your Plaque program and would be willing to share your story, please let me know by commenting below. While losing half your body weight is not necessarily a requirement for health, it makes an incredibly inspiring story for others.

If we use your story, I will set aside a copy of my soon-to-be-released book, Wheat Belly.

Lp(a): Be patient with fish oil

High-dose omega-3 fatty acids from fish oil has become the number one strategy for reduction of lipoprotein(a), Lp(a), in the Track Your Plaque program for gaining control over coronary plaque and heart disease risk.

The original observations made in Tanzanian Bantus in the Lugalawa Study by Marcovina et al first suggested that higher dietary exposure to fish and perhaps omega-3 fatty acids from fish were associated with 40% lower levels of Lp(a). Interestingly, higher omega-3 exposure was also associated with having the longer apo(a) "tails" on Lp(a) molecules, a characteristic associated with more benign, less aggressive plaque-causing behavior.

Of course, the 600+ fish- consuming Bantus in the study consumed fish over a lifetime, from infancy on up through adulthood. So what is the time course of response if us non-Bantus take higher doses of fish oil to reduce Lp(a)?

We have been applying this approach in the Track Your Plaque program and in my office practice for the past few years. To my surprise, the majority of people taking 6000 mg per day of omega-3 fatty acids, EPA and DHA, will drop Lp(a) after one year.  Some have required two years.  Therefore checking Lp(a) after, say, 3 or 6 months, is nearly useless. (An early response does, however, appear to predict a very vigorous 1-2 year response.)

I'm sure that there is an insightful lesson to be learned from the incredibly slow response, but I don't currently know what it is.  But this strategy has become so powerful, despite its slow nature, that it has allowed many people to back down on niacin.

Baby your pancreas

There it is, sitting quietly tucked under your diaphragm, nestled beneath layers of stomach and intestines, doing its job of monitoring blood sugar, producing insulin, and secreting the digestive enzymes that allow you to convert a fried egg, tomato, or dill pickle into the components that compose you.

But, if you've lived the life of most Americans, your pancreas has had a hard life. Starting as a child, it was forced into the equivalent of hard labor by your eating carbohydrate-rich foods like Lucky Charms, Cocoa Puffs, Hoho's, Ding Dongs, Scooter Pies, and macaroni and cheese. Into adolescent years and college, it was whipped into subservient labor with pizza, beer, pretzels, and ramen noodles. As an adult, the USDA, Surgeon General's office and other assorted purveyors of nutritional advice urged us to cut our fat, cholesterol, and eat more "healthy whole grains"; you complied, exposing your overworked pancreas to keep up its relentless work pace, spewing out insulin to accommodate the endless flow of carbohydrate-rich foods.

So here we are, middle aged or so, with pancreases that are beaten, worn, hobbling around with a walker, heaving and gasping due to having lost 50% or more of its insulin-producing beta cells. If continued to be forced to work overtime, it will fail, breathing its last breath as you and your doctor come to its rescue with metformin, Actos, Januvia, shots of Byetta, and eventually insulin, all aimed at corralling the blood sugar that your failed pancreas was meant to contain.

What if you don't want to rescue your flagging pancreas with drugs? What if you want to salvage your poor, wrinkled, exhausted pancreas, eaking out whatever is left out of the few beta cells you have left?

Well, then, baby your pancreas. If this were a car with 90,000 miles on it, but you want it to last 100,000, then change the oil frequently, keep it tuned, and otherwise baby your car, not subjecting it to extremes and neglect to accelerate its demise. Same with your pancreas: Allow it to rest, not subjecting it to the extremes of insulin production required by carbohydrate consumption. Don't expose it to foods like wheat flour, cornstarch, oats, rice starch, potatoes, and sucrose that demand overtime and hard labor out of your poor pancreas. Go after the foods that allow your pancreas to sleep through a meal like eggs, spinach, cucumbers, olive oil, and walnuts. Give your pancreas a nice back massage and steer clear of "healthy whole grains," the nutritional equivalent of a 26-mile marathon. Pay your pancreas a compliment or two and allow it to have occasional vacations with a brief fast.

Bread equals sugar

Bread, gluten-free or gluten-containing, in terms of carbohydrate content, is equivalent to sugar.

Two slices of store-bought whole grain bread, such as the gluten-free bread I discussed in my last post, equals 5- 6 teaspoons of table sugar:








 

 

 

 

 

 

 

 

Some breads can contain up to twice this quantity, i.e., 10-12 teaspoons equivalent readily-digestible carbohydrate.

Gluten-free carbohydrate mania

Here's a typical gluten-free product, a whole grain bread mix. "Whole grain," of course, suggests high-fiber, high nutrient composition, and health.



 

 

 

 

 

 

 

 

What's it made of? Here's the ingredient list:
Cornstarch, Tapioca Starch, Whole Grain Sorghum Flour, Whole Grain Teff Flour, Whole Grain Amaranth Flour, Soy Fiber, Xanthan Gum, Soy Protein, Natural Cocoa and Ascorbic Acid

In other words, carbohydrate, carbohydrate, carbohydrate, carbohydrate and some other stuff. It means that a sandwich with two slices of bread provides around 42 grams net carbohydrates, enough to send your blood sugar skyward, not to mention trigger visceral fat formation, glycation, small LDL particles and triglycerides.

Take a look at the ingredients and nutrition facts on the label of any number of gluten-free products and you will see the same thing. Many also have proud low-fat claims.

This is how far wrong the gluten-free world has drifted: Trade the lack of gluten for a host of unhealthy effects.

Gluten-free is going DOWN

The majority of gluten-free foods are junk foods.

People with celiac disease experience intestinal destruction and a multitude of other inflammatory conditions due to an immune response gone haywire. The disease  is debilitating and can be fatal unless all gliadin/gluten sources are eliminated, such as wheat, barley, and rye.

A gluten-free food industry to provide foods minus gliadin/gluten has emerged, now large enough to become an important economic force. Even some Big Food companies are getting into the act, like Kraft, that now lists foods they consider gluten-free.

So we have gluten-free breads, cupcakes, scones, pretzels, breakfast cereals, crackers, bagels, muffins, pancake mixes and on and on. All are made with ingredients like brown rice flour, cornstarch, tapioca starch, and potato starch. Occasionally, they are made with amaranth, teff, or quinoa, other less popular, but gluten-free, grains.

Problem: These gluten-free ingredients, while lacking gliadin and gluten, make you fat and diabetic. They increase visceral fat, cause blood sugar to skyrocket higher than nearly all other foods (even higher than wheat, which is already pretty bad), trigger formation of small LDL and triglycerides, and are responsible for exaggerated postprandial (after-eating) lipoprotein distortions. They cause heart disease, cataracts, arthritis, and a wide range of other conditions, all driven by the extreme levels of glycation they generate.

Eliminating all things wheat from the diet is one of the most powerful health strategies I have ever witnessed. But replacing lost wheat with manufactured gluten-free foods is little better than replacing your poppyseed muffin with a bowl of jelly beans.

Whenever we've relied on the food industry to supply a solution, they've managed to bungle it. Saturated fat was replaced with hydrogenated fat and polyunsaturates; sucrose replaced with high-fructose corn syrup. Now, they are replacing wheat gluten-containing foods with junk carbohydrates.

For this reason, I am bringing out a line of recipes and foods that will be wheat gliadin/gluten-free, do NOT contain the junk carbohydrates that gluten-free foods are made of, and are genuinely healthy. They are tasty, to boot.

The gluten-free industry needs to smarten up. Having a following that is free of cramps and diarrhea but are obese, diabetic, and hobbling on arthritic knees and hips is good for nobody.

Medicine ain't what it used to be

The practice of medicine ain't what it used to be.

For instance:

White coats are out-of-date--Not only do they serve as filthy reservoirs of microorganisms (since they hang unwashed after repeated use week after week), they only serve to distance the practitioner from the patient, an outdated notion that should join electroshock therapy to treat homosexuality and other "disorders" in the museum of outdated medical practices.

Normal cholesterol panel . . . no heart disease?

I often hear this comment: "I have a normal cholesterol panel. So I have low risk for heart disease, right?"

While there's a germ of truth in the statement, there are many exceptions. Having "normal" cholesterol values is far from a guarantee that you won't drop over at your daughter's wedding or find yourself lying on a gurney at your nearest profit-center-for-health, aka hospital, heading for the cath lab.

Statistically, large populations do indeed show fewer heart attacks at the lower end of the curve for low total and  LDL cholesterol and the higher end of HDL. But that's on a population basis. When applied to a specific individual, population observations can fall apart. Heart attack can occur at the low risk end of the curve; no heart attack can occur at the high risk end of the curve.

First of all, to me a "normal" lipid panel is not adhering to the lax notion of "normal" specified in the lab's "reference range" drawn from population observations. Most labs, for instance, specify that an HDL cholesterol of 40 mg/dl or more and triglycerides of 150 mg/dl or less are in the normal ranges. However, heart disease can readily occur with normal values of, say, an HDL of 48 mg/dl and triglycerides of 125 mg/dl, both of which allow substantial small oxidation-prone LDL particles to develop. So "normal" may not be ideal or desirable. Look at any study comparing people with heart disease vs. those without, for instance: Typical HDLs in people with heart attacks are around 46 mg/dl, while HDLs in people without heart attacks typically average 48 mg/dl--there is nearly perfect overlap in the distribution curves.

There are also causes for heart disease that are not revealed by the lipid values. Lipoprotein(a), or Lp(a), is among the most important exceptions: You can have a heart attack, stroke, three stents or bypass surgery at age 40 even with spectacular lipid values if you have this genetically-determined condition. And it's not rare, since 11% of the population express it. How about people with the apo E2 genetic variation? These people tend to have normal fasting cholesterol values (if they have only one copy of E2, not two) but have extravagant abnormalities after they eat that contribute to risk. You won't know this from a standard cholesterol panel.

Vitamin D deficiency can be suggested by low HDL and omega-3 fatty acid deficiency suggested by higher triglycerides, but deficiencies of both can exist in severe degrees even with reasonably favorable ranges for both lipid values. Despite the recent inane comments by the Institute of Medicine committee, from what I've witnessed from replacing vitamin D to achieve serum 25-hydroxy vitamin D levels of 60-70 ng/ml, vitamin D deficiency is among the most powerful and correctable causes of heart disease I've ever seen. And, while greater quantities of omega-3 fatty acids from fish oil are associated with lower triglycerides, they are even better at reducing postprandial phenomena, i.e., the after-eating flood of lipoproteins like VLDL and chylomicron remnants, that underlie formation of much atherosclerotic plaque--but not revealed by fasting lipids.

I view standard cholesterol panels as the 1963 version of heart disease prediction. We've come a long way since then and we now have far better tools for prediction of heart attack. Yet the majority of physicians and the public still follow the outdated notion that a cholesterol panel is sufficient to predict your heart's future. Nostalgic, quaint perhaps, but as outdated as transistor radios and prime time acts on the Ed Sullivan show.

 

Idiot farm

The notion of genetic modification of foods and livestock is a contentious issue. The purposeful insertion or deletion of a gene into a plant or animal's genome to yield specific traits, such as herbicide resistance, nutritional composition, or size, prompted the Codex Alimentarius Commission, an international effort to regulate the safety of foods, to issue guidelines concerning genetically-modified foods.

The committee is aware of the concept of unintended effects, i.e., effects that were not part of the original gene insertion or deletion design. In their report, last updated in 2009, they state that:

Unintended effects can result from the random insertion of DNA sequences into the plant genome, which may cause disruption or silencing of existing genes, activation of silent genes, or modifications in the expression of existing genes. Unintended effects may also result in the formation of new or changed patterns of metabolites. For example, the expression of enzymes at high levels may give rise to secondary biochemical effects or changes in the regulation of metabolic pathways and/or altered levels of metabolites.

They make the point that food crops generated using techniques without genetic modification are released into the food supply without safety testing:

New varieties of corn, soybean, potatoes and other common food plants are evaluated by breeders for agronomic and phenotypic characteristics, but generally, foods derived from such new plant varieties are not subjected to the rigorous and extensive food safety testing procedures, including studies in animals, that are typical of chemicals, such as food additives or pesticide residues, that may be present in food.

In other words, conventional plant breeding techniques, such as hybridization, backcrossing, and introgression, practices that include crossing parental plants with their progeny over and over again or crossing a plant with an unrelated plant, yield unique plants that are not subject to any regulation. This means that unintended effects that arise are often not identified or tested. Plant geneticists know that, when one plant is crossed with another, approximately 5% of the genes in the offspring are unique to that plant and not present in either parent. It means that offspring may express new characteristics, such as unique gliadin or gluten proteins in wheat, not expressed in either parent and with new immunological potential in consuming humans.

Dr. James Maryanski, the FDA's Biotechnology Coordinator, stated during Congressional testimony in 1999 that:

The new gene splicing techniques are being used to achieve many of the same goals and improvements that plant breeders have sought through conventional methods. Today's techniques are different from their predecessors in two significant ways. First, they can be used with greater precision and allow for more complete characterization and, therefore, greater predictability about the qualities of the new variety. These techniques give scientists the ability to isolate genes and to introduce new traits into foods without simultaneously introducing many other undesirable traits, as may occur with traditional breeding. [Emphasis mine.]

Efforts by the Codex Alimentarius and FDA are meant to control the introduction and specify safety testing procedures for genetically modified foods. But both organizations have publicly stated that there is another larger problem that has not been addressed that predates genetic modification. In other words, conventional methods like hybridization techniques, the crossing of different strains of a crop or crossing two dissimilar plants (e.g., wheat with a wild grass) have been practiced for decades before genetic modification became possible. And it is still going on.

In other words, the potential hazards of hybridization, often taken to extremes, have essentially been ignored. Hybridized plants are introduced into the food supply with no question of human safety. While hybridization can yield what appear to be benign foods, such as the tangelo, a hybrid of tangerines and grapefruit, it can also yield plants containing extensive unintended effects. It means that unique immunological sequences can be generated. It might be a unique gliadin sequence in wheat or a unique lectin sequence in beans. None are tested prior to selling to humans. So the world frets over the potential dangers of genetic modification while, all along, the much larger hazard of hybridization techniques have been--and still are--going on.

Imagine we applied the hybridization techniques applied by plant geneticists to humans, mating an uncle with his niece, then having the uncle mate again with the offspring, repeating it over and over until some trait was fully expressed. Such extensive inbreeding was practiced in the 19th century German village of Dilsberg, what Mark Twain described as "a thriving and diligent idiot factory."

Eat triglycerides

Dietary fats, from olive oil to cocoa butter to beef tallow, are made of triglycerides.

Triglycerides are simply three ("tri-") fatty acids attached to a glycerol backbone. Glycerol is a simple 3-carbon molecule that readily binds fatty acids. Fatty acids, of course, can be saturated, polyunsaturated, and monounsaturated.

Once ingested, the action of the pancreatic enzyme, pancreatic lipase, along with bile acids secreted by the gallbladder, remove triglycerides from glycerol. Triglycerides pass through the intestinal wall and are "repackaged" into large complex triglyceride-rich (about 90% triglycerides) molecules called chylomicrons, which then pass into the lymphatic system, then to the bloodstream. The liver takes up chylomicrons, removes triglycerides which are then repackaged into triglyceride-rich very low-density lipoproteins (VLDL).

So eating triglycerides increases blood levels of triglycerides, repackaged as chylomicrons and VLDL.

Many physicians are frightened of dietary triglycerides, i.e, fats, for fear it will increase blood levels of triglycerides. It's true: Consuming triglycerides does indeed increase blood levels of triglycerides--but only a little bit. Following a fat-rich meal of, say, a 3-egg omelet with 2 tablespoons of olive oil and 2 oz whole milk mozzarella cheese (total 55 grams triglycerides), blood triglycerides will increase modestly. A typical response would be an increase from 60 mg/dl to 80 mg/dl--an increase, but quite small.

Counterintuitively, it's the foods that convert to triglycerides in the liver that send triglycerides up, not 20 mg/dl, but 200, 400, or 1000 mg/dl or more. What foods convert to triglycerides in the liver? Carbohydrates.

After swallowing a piece of multigrain bread, for instance, carbohydrates are released by salivary and gastric amylase, yielding glucose molecules. Glucose is rapidly absorbed through the intestinal tract and into the liver. The liver is magnificently efficient at storing carbohydrate calories by converting them to the body's principal currency of energy, triglycerides, via the process of de novo lipogenesis, the alchemy of converting glucose into triglycerides for storage. The effect is not immediate; it may require many hours for the liver to do its thing, increasing blood triglycerides many hours after the carbohydrate meal.

This explains why people who follow low-fat diets typically have high triglyceride levels--despite limited ingestion of triglycerides. When I cut my calories from fat to 10% or less--a very strict low-fat diet--my triglycerides are 350 mg/dl. When I slash my carbohydrates to 40-50 grams per day but ingest unlimited triglycerides like olive oil, raw nuts, whole milk cheese, fish oil and fish, etc., my triglycerides are 50 mg/dl.

Don't be afraid of triglycerides. But be very careful with the foods that convert to triglycerides: carbohydrates.

 

 

 

 

 

 

 
You could take vitamin D or . . .

You could take vitamin D or . . .

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.

Comments (53) -

  • DS

    8/26/2011 12:23:02 PM |

    Do you take the 8,000 units *daily*?  I started out with a serum vitamin D level of 12 ng/ml and was prescribed 50,000 units per *week*.  That got me up to 27 ng/ml (which the doctor considered acceptable).  At that point, a different doctor advised me to take 1,000 units a day, but I started taking 2,000 units and have now reached 60 ng/ml.  I was concerned that 2,000 might be excessive, and now that I have reached a good level of serum D, I thought maybe I should cut back to 1,000.  But you take 8,000 daily?

  • Johan

    8/26/2011 1:10:12 PM |

    D.S. 8000 daily x 7 days = 56000 weekly, not all that different from 50000 weekly.

  • Steve Cooksey

    8/26/2011 1:22:15 PM |

    Love the post Dr. Davis.
    I have NOT been sick in 2+ years... seriously.  I tell people, I don't know if it's the 'low carb primal' meal plan ... or the almost daily exercise ... or the daily D3.  Most likely a combination of all 3. Smile   I take 4-8k daily depending on the season and 'sunlight' exposure.

    Thriving!... not just surviving.

    Steve

  • Melissa

    8/26/2011 1:23:10 PM |

    This may be another case of everyone being different. Over the course of three years on 2,000, then 4,000 units a day I got to 48 then 63 ng/ml. When I upped it to 6,000 units I hit exactly 100 ng/ml. When I was at the lower levels I felt fantastic, at 100 I did not.  I recommend frequent testing to see what amount brings you to the ideal level and keeps you there.

  • majkinetor

    8/26/2011 1:33:59 PM |

    Would it be beneficial to take K2 along with D3 just in case ?
    Vitamin D boosts calcium availability and I wouldn't want it to finish on wrong places.

  • Mary Titus

    8/26/2011 1:58:46 PM |

    Yes, K2, magnesium and zinc should also be taken if you  suspect that your diet might be low in these. I discovered that I do not absorb supplements very well unless they are in liquid form.

  • Dr. William Davis

    8/26/2011 5:07:44 PM |

    DS and Johan--

    Be careful: You're confusing cholecalciferol (D3), the human form of vitamin D, with ergocalciferol (D2), the non-human plant or mushroom form.

    Vitamin D is a (pro)hormone. Humans should ONLY take the human form, never the plant form. For one thing, 50,000 units of D2 is apprximately equivalent to 15,000 units D3, because it's different. It is inferior.

    If a doctor prescribes D2, it's because he has no idea what he/she is doing. There is absolutely NO reason to favor D2 over D3.

  • Dr. William Davis

    8/26/2011 5:08:35 PM |

    Great, Steve!

    I've personally been enjoying the same experience.

  • Dr. William Davis

    8/26/2011 5:12:11 PM |

    Absolutely. Checking every 6 months has worked out very well for us.

  • Renfrew

    8/26/2011 5:15:29 PM |

    There are reports that high intake of D3 will cause calcification of arteries and heart valves. The reported levels are over 50-60 ng in the serum D3. So there seems to be s diminishing effect of high D3 intake. Also it seems that taking K2 will mitigate or offset this effect. There are conflicting reports on this though. Any thoughts?
    Renfrew

  • Dana

    8/26/2011 5:39:15 PM |

    That's true of the plant forms of all the fat-soluble vitamins.  We have been badly misled.

    The statistics and study summaries I've read seem to indicate that somewhere between 40 and 50 percent of the population cannot convert beta carotene to vitamin A in large enough amounts for BC to be useful as an A source.  If the respondents in those studies were only healthy people, the total percentage is far higher;  diabetics and hypothyroid people can't make the conversion.  And that's only adults.  Infants and young children can't make the conversion either, which pushes the percentage even higher.  Vitamin A has many tasks it performs in the growing fetus; helping the urinary tract develop is one of those tasks.  The Mayo Clinic tells us on its website that urinary tract defects are the most common class of defects in the United States.  Vitamin A is also important in eye and tooth enamel development, among the many, many other functions it performs.  How many people are walking around with eyeglasses, and how many young children are getting cavities now?

    The Rotterdam study showed that vitamin K1 in plants does nothing to mitigate heart disease risk, whereas K2 from animal organs and dairy does.  I have heard from other sources that the K2 in natto (mk-7) does not cross the placenta, telling me it's less important to our health than the K2 from organs and dairy (mk-4 or menatetrenone).  K2/mk-4 is important in insulin sensitivity as well as heart health and bone and tooth strength.  But most experts focus on K1 or on the K2 in natto, to our detriment.

    A, D, and K are so vitally important to good physical development and avoiding chronic disease.  The information is out there, in study after study.  If the experts won't admit to it, we need to educate ourselves.

  • Dana

    8/26/2011 5:43:21 PM |

    100 ng/ml is too high for anybody.  Dr. Davis probably hits the high end of acceptable.  No wonder you felt bad.

  • Dana

    8/26/2011 5:47:37 PM |

    I insist on supplementing three of the four fat-soluble vitamins because I've found out the hard way that the plant precursors of those vitamins DO NOT work well for me.  I suspect my experience is more in the majority than the minority, too.  Here's my regimen:

    Vitamin A from fish liver oil (read the label):  8000 IU
    Vitamin D3: 5000 IU
    Vitamin K2, analog mk-4 (menatetrenone): 1-5 drops of a liquid supplement in MCT oil.  This company suggests taking 15 drops a day, which is over 10,000 of the recommended daily intake, and I see no point in going that high.

    If I could afford no other supplements, I always take these.  I suffered from a subclinical (at least according to mainstream medical practice) vitamin A deficiency from 2004 on up to 2007 or 2008 that manifested as reproductive health problems and also birth defects in my daughter.  No one suspected an A shortage as the problem.  I figured it out by happy accident.  I am apparently not a good converter of beta carotene and my daughter paid the price.  I don't like liver, and dairy and eggs are not high enough in the vitamin, so this is what I do.  And this way the vitamins all work together synergistically  and I don't have to worry about toxicity.

  • DS

    8/26/2011 6:20:09 PM |

    Yeah, I know, but I was taking 50,000 units weekly to rectify a profound *deficiency*, not as a maintenance dose.

  • DS

    8/26/2011 6:30:06 PM |

    I don't know if it was D2 or D3 when I was taking 50,000 units per week (by prescription; this was over a year ago), but the 2,000 units (OTC) I now take daily are D3.  If this dose has me maintained at 60 ng/ml, it's amazing how the 8,000 units you (Dr. Davis) take isn't too much.  I guess this goes to show that monitoring is crucial, and there's no one-size-fits-all in supplements.

  • Don

    8/27/2011 12:51:54 AM |

    vit D and sleep apnea
    http://www.musclechatroom.com/forum/showthread.php?18736-quot-Vitamin-quot-D-is-a-Hormone.-It-Cures-Sleep-disorders-amp-many-ailments

  • Gene K

    8/27/2011 1:11:11 AM |

    Long time followers of this blog will recall that Dr Davis has discussed vitamin D and K2-related issues many times here. You can find many answers to your questions by following the search links http://www.trackyourplaque.com/blog/category/vitamin-d and http://www.trackyourplaque.com/blog/category/vitamin-k2. Not all posts will be directly related to this discussion, but you will know what is related and what is not.

  • The Health Magazine

    8/27/2011 4:29:06 AM |

    I guess Vit D can also be gained freely from the nature.

  • Might-o'chondri-AL

    8/27/2011 5:51:18 AM |

    To Jack K. ... posted here since Server blocked this where belongs.
    Hi Jack K.,
    You once mentioned being ApoE4 (I think), thus are specially interested; and are in your "prime" dedicated to physical culture. Frankly I have no insight into how modified fasting or limiting snack fuel would let a body builder achieve their goals. (Doc recently stated how hard it was for athletes to restrict quick energy foods, like carbs.)

    HDL heritability  in the Dutch ERASMUS study was put at 43% and the study of isolated Italian's from Linosa put HDL heritability at 54% (and for those Italians having both high triglycerides and low HDL that dual heritability was 31%). When one considers the ApoA2 percentage in HDL in relation to the amount of ApoA1 in HDL then that detail is going to involve the copy number of ApoA2 genes the individual has; and what is eaten, but not the type of protein one chooses, because it is more lipids (as fatty acid derivatives) that are involved in key signaling roles.

    Doc & others ( ex: WholeHealthSource) tell us saturated fat intake boosts total cholesterol, but more so HDL than LDL; conversely when restrict saturated fat HDL level falls . For those with ApoE4 however Doc repeatedly has mentioned that for them it may be best to decidedly limit fat. In which case triglyceride levels are seemingly something one must work around.

    Restricting saturated fat intake sees a decrease in  ApoA1 because without those fatty acid derivatives (lipid signalers) ApoA1 undergoes more breakdown, and in addition there is less ApoA1 secretion (not only does ApoA1 degrade faster than ApoA2 but the kidneys apparently don't excrete ApoA2, like the kidneys do to ApoA1). This is how statistically low HDL is associated with a higher percentage of ApoA2  in it's make up. Yet genetics can conceivably tweak this dynamic because fatty acid derivatives (lipid signalers) have to up-regulate PPAR alpha (subject to genetic variation), which then acts on the ApoA2 gene regulatory  element "J" (subject to genetic variation) before ApoA2 gets made in the liver (& a bit in intestine).

    Experimentally when PUFA  made up 40% of total dietary fat intake there was less measurable ApoA1 mRNA & less liver secretion of ApoA1; while if 30% of total dietary fat is mono-saturated & PUFA there is usually no change in amount of ApoA1 mRNA, nor less liver secretion of ApoA1. When diet is classified as low fat and fat only 9% of total calorie intake ApoA1 levels usually decrease; I don't know if this is the fat level Doc advises his ApoE4 patients to try. I am not aware of any relevance of dietary protein to ApoA1 levels; however there is some recent indication that iso-flavone plant phyto-sterols (ex: genisten & daidzein from soy) may alter ApoA1 & ApoA2 levels (in contrast to older studies showing no benefit). I garnish food with a dry palmfull of Japanese black soy  fermented 1 year in Koji, called "Tochi", specially imported from Japan for Japanese restaurants by Miyako Foods  626-962-9633 (no financial interest for me); they also make this into a nice specialty miso - but I do not know how it compares in iso-flavone content to other soy forms.

    2011:  Male rhesus monkey's  ApoA1 g/l went up from 2.34 when fed soy stripped of iso-flavones to 2.75 when their soy had iso-flavones; and their ApoA2 g/l went up from 0.20 when fed  iso-flavone free soy to 0.22 when their soy had iso-flavones....Female rhesus monkey's ApoA1 g/l went from 2.19 when fed iso-flavone free soy to 2.75 when fed soy with iso-flavones; and their ApoA2 g/l went up from 0.16 on iso-flavone free soy to 0.19 on soy containing iso-flavones. (As for Lipo-a : that also went down with iso-flavones.) The female 15% boost in HDL (90% of HDL = ApoA1 + ApoA2) being greater than the males is attributed to the fact that some of the males went from pre-puberty to puberty during experiment and there are often sex related variations in HDL; and to be precise the authors stipulate that iso-flavones may not work the same when the subject has either familial hyper-cholesterol or those with ApoE4.

    Doc has given those with ApoE4 and low HDL a little appreciated strategy when he exhorts them not to eat oats, potatoes and wheat bread; these are common foods that increase levels of an asymmetrical lipid called lyso-phosphatidyl-choline (lysoPC). Remember that HDL also contains glycero-phospho-lipids; well, inside a cell the enzyme cPLA2 (cytosolic phospholipase A2) spins off phospho-lipids (another fatty acid derivative). And unfortunately it is usually individuals with low HDL tend to have more lysoPC than normal; which is considered pro-atherogenic when the lysoPC is configured in a "bad" molecular form (and yet other "good" lysoPC  configurations carry desirable DHA across the brain blood barrier).

    It was shown that eating fatty fish 4-5 times a week decreases the total level of lysoPC, and both lowers the amount of  "bad" lysoPC, while raising the "good" configurations of lysoPC; which is another reason to follow Doc's high fish oil suggestion (inter-daily fatty fish might be a lot of mercury intake). I believe Doc is allowing fish oil and  maybe some fish for his ApoE4 patients. This experiment ruled out saturated fat beneficially influencing those lysoPC  molecular variations because subjects avoided all dairy fat, cream or butter.

    The lysoPC that is carried in oxidized LDL molecules negatively affects one's tricky macrophages and also the smooth muscle cells of the artery; lyso-lipids not only invoke signals but can themselves be transformed. Certain lysoPC  yield a lot of  the platelet activating factor (alkyl-acetyphosphatidyl-choline) which contributes to sustaining inflammation, and so sets stage for atherosclerotic plaque. High levels of HDL usually conveniently equates with reduced levels of TNF alpha, a condition resulting in fewer undesirable adhesion proteins on the blood vessel's endothelium;  so, conversely those individuals with ApoE4 related low HDL are statistically prone to more endothelial adhesion proteins, and thus should try to do what they can to keep as much "bad" lysoPC controlled with diet.

  • Dr. William Davis

    8/27/2011 2:17:05 PM |

    Precisely, DS. I've got people who require 20,000 units to achieve this blood level, I've got a rare person who needs none.

    The individual variation in need is quite wide. That's why the concept of an RDA for this hormone is, in a word, absurd.

  • Mike

    8/27/2011 3:30:42 PM |

    I find that even low doses of vitamin D leave me feeling terrible. I get these weird chest pains and lower back pain as well. It also causes pretty bad breakouts for me. I've tried different preparations and brands but it all ends up leading to the same symptoms. This usually happens after I've accumulated a couple of weeks of supplement usage. I haven't experimented with different dosing strategies yet(weekly, bi-weekly or even monthly). I made sure to supplement with magnesium and K2 as well. It sucks because I really like all of the preventative benefits that D3 has to offer but it just doesn't seem to agree with me.
    Mike

  • Joe

    8/27/2011 4:41:48 PM |

    Dr. Davis:

    Any chance that you'll be writing more about the positive results you're seeing in your clinic from increased doses of vitamin D on aortic insufficiency?

    Joe

  • majkinetor

    8/27/2011 8:51:55 PM |

    Since D activates immune function a lot, could it be that you have some chronic infection and effects you are experiencing are because of bacterial endotoxins which are released when bacteria dies ?

    Have you done the D test ?

    If so, perhaps taking some detox supplement would help like huge doses of Vitamin C, clay, NAC etc...

  • Dr. William Davis

    8/27/2011 10:39:35 PM |

    Sure, good idea. However, the majority of experiences have been in aortic stenosis, not insufficiency, only because I've got about 10 people with stenosis for every 1 with insufficiency--just too uncommon.

  • Dr. William Davis

    8/27/2011 10:41:04 PM |

    Hi, Mike--
    Sorry about your struggles. I've seen this once or twice, but I'm not sure about why. You might ask your doctor to at least investigate parathyroid and adrenal status, e.g., PTH, calcium, and salivary cortisols. These might booby trap a vitamin D effort. After all, taking vitamin D should be no more dangerous than getting a nice tan.

  • Mike

    8/27/2011 11:48:55 PM |

    Are you suggesting that my reaction could be from some sort of bacterial "die off?"

    Interesting. I never really thought about it. I did get my levels checked during the few months I was supplementing and it was only 52ng/ml.

  • Jean

    8/28/2011 2:20:12 AM |

    Mike, are you getting enough quality Vitamin A? Vitamin A and D work together. Chris Masterjohn had a post about it on the Weston A. Price website, they have a lot of info there about A and D levels and how they work together. Other people have had reactions to D also and found that they deficient in A, mostly, I think, by evaluating their diet and seeing there were few good sources of A there. Also, older people and some just not so lucky folks don't process beta carotene into vitamin A, it's age and genetics.

  • Mike

    8/28/2011 2:49:48 AM |

    It was recommended that I take additional magnesium and vitamin k2 to see if it would make a difference. I've never taken additional vitamin A though because according to the  vitamin d council, additional vitamin A can be toxic.

    I have read that Masterjohn article before though.

  • Jennifer

    8/28/2011 1:55:19 PM |

    I just wanted to add my experience on Vit. D3 supplementation.

    Two years ago in July I started supplementing 5,000 i.u. Vit. D3 a day.  My sister had been found low, I live relatively the same lifestyle, and thought, "what the heck, I'll start and get my blood tested in late winter next year".  

    That next March I had a blood test and found my blood levels to be at a whopping  32 ng/ml.  My doctor said "fine, you're within range" and I thought, "no, that's not fine" and started to take 15,000 i.u. a day.  In March again this year I had a blood draw, and expected to see a very high ng/ml of Vit. D.  My actual result?  It had raised to 45 ng/ml.  I was floored that with that amount, my levels had only raised such a small amount.  

    I will add that I am obese.   I just wanted to give you my experience with D3 supplementation in case it helps someone else.  I have now upped my supplementation once more to 20,000 i.u. a day, and if my next blood test is appreciably better, will hold at that level or drop back some.  I will add that I haven't had many if any colds this past year, so even if I have not attained a more optimal level (perhaps I can't due to obesity)  it's still doing me a lot of good.

  • Mike

    8/28/2011 2:50:22 PM |

    Oh, I forgot to mention. A friend of mine suggested I try applying liquid vitamin D on my skin and then checking to see if that raises/maintains my blood levels.

    I'm thinking about applying 5 to 8k per day to the skin AFTER I shower so that it gets plenty of time to absorb in the skin. Then re-test my levels after a few months to see if it works.

  • Dr. William Davis

    8/29/2011 12:09:27 PM |

    Please let me know what becomes of your experience! We've not tried this specific strategy.

  • Dr. William Davis

    8/29/2011 12:10:53 PM |

    Hi, Jennifer--

    Yes, indeed: The individual experiences with vitamin D can vary widely. You may also note that, 3 or so years into the experience, your needs will diminish, sometimes dramatically, with less vit D required to generate the same blood level.

  • Linda

    8/30/2011 3:55:38 PM |

    I began experiencing tightness and soreness in my hips and lower back this year. Have been low carbing for over three years, and, except for a short period of stupidity earlier this year, have not consumed any flour products. My multi-vitamin contains only 500 IU of D3, so I am adding this to my daily supplementing. Should I start slowly, 1000 IU a day for a month, and slowly increase? Is D3 toxic? BTW I am in my late 60's, and I do exercise 5-6 days a week as well.

  • hggh2

    8/30/2011 5:23:55 PM |

    I have read that 20-25ng/ml is optimal.
    "Although numerous studies have not
    observed any adverse effects of higher
    vitamin D status, a few have. Historically,
    the main health risks associated with
    excessive vitamin D are linked with
    abnormal plasma calcium concentrations.
    Excessive vitamin D is recognized to
    cause hypercalcemia by increasing intestinal
    calcium absorption or by increasing
    mobilization of bone calcium. Although
    hypercalcemia is uncommon with intakes
    less than 10 000 IU/d,3 knowledge of
    non-calcium-related adverse events is
    limited. At least some evidence suggests
    that high vitamin D status may be associated
    with increased risk of some cancers.
    In a large case control study of prostate
    cancer in Finland and Norway, both
    low (32 ng/mL)
    25(OH)D concentrations were reported
    to be associated with an increased incidence
    of prostate cancer (50% and 70%,
    respectively) compared with individuals
    with serum 25(OH)D concentrations
    between 16 and 24 ng/mL.4 A direct relationship
    between higher vitamin D status
    and the development of esophageal
    carcinoma also has been observed in
    Chinese men.5 Interestingly, all the participants,
    including those in the highest
    quintile, were vitamin D deficient (26.2
    ng/mL) with a 3-fold increased risk of
    pancreatic cancer compared to individuals
    with the lowest baseline status (<12.8
    ng/mL). Overall, these studies suggest
    there may be an optimum status and that
    values below or above may increase risk
    of certain types of cancer.
    Adverse events associated with high vitamin
    D status other than cancer also have
    been observed. Recent data from large
    epidemiologic studies, including the Third
    National Health and Nutrition Examination
    Survey (NHANES III) and the Framingham
    Heart Study, suggest that a “U-shaped
    curve” relationship exists with all-cause
    mortality and the incidence of cardiovascular
    disease because both low and high
    25(OH)D concentrations elevated risk.7,8
    In the NHANES III study, higher mortality
    risk was observed in participants
    with 25(OH)D above 49 ng/mL. In the
    Framingham study, the lowest cardiovascular
    disease risks were found in
    participants with baseline 25(OH)D levels
    of 20 to 25 ng/mL but increased with both
    lower and higher values,8 thus suggesting
    that increased cardiovascular risk occurred
    at levels below 30 ng/mL. Furthermore,
    the optimal 25(OH)D levels for protection
    against cardiovascular disease and certain
    types of cancer may differ from those
    for bone metabolism or normal parathyroid
    hormone physiology."
    from 'too much.pdf' in http://is.gd/vT4Ogh Studies from DrGreger collection.

    DrGreger has since changed his recommendation from 4000IU to 2000IU/day:
    http://www.facebook.com/NutritionFacts.org/posts/193068787424836 yesterday's update

  • Dr. William Davis

    8/30/2011 6:42:20 PM |

    As knowledge marches forward, there will always be differing observations made, some good, some bad, some indifferent.

    However, if we weigh the totality of evidence (and I throw in my experience that now amounts to several thousand patients), there has never been any strategy as powerful as vitamin D--except for elimination of wheat in the human diet, the two most spectacular new health strategies I have encountered in my career.

  • Johnt

    8/31/2011 1:51:15 AM |

    what happened to my post?

  • Johnt

    9/2/2011 4:04:32 PM |

    I posted 30Aug11 about a concern I have concerning D3 toxicity, but the message disappeared. I have been following for some two years a daily D3 regimen (4000-8000mg) without incident. I recently experienced unusual chest pains over a week and ended up getting a thorough checkup which found no apparent heart problems. However upon disclosing my protracted D3 intake (considered “very high!") it was suggested I suspend D3 for awhile on the off chance D3 toxicity may be the source of my symptoms. I was wondering if anyone else here has had this experience. As I look into this more, I have learned that D3 toxicity is more subtle and prevalent than I had thought, and is not something to be taken lightly. Clearly as Dr Davis has cautioned, adjusting to the right dosage varies from person to person, and given the latent build up of D3 in fat tissue over time, it is not as straight forward getting it right as one might think. In my case the jury is still out.

  • Johnt

    9/2/2011 4:08:38 PM |

    re previous message: 4000-8000 mg = 4000-8000iu's

  • Michelle

    9/7/2011 5:25:07 PM |

    I swear by vitamin D3. It helps me avoid asthma flare ups and kick bugs before they can make me wheeze. In the warm months, I make sure to get outside as much as possible as there are other things produced by the sun in addition to Vitamin D, some of which may be important. Then in the winter, I supplement 2-5k ius a day, increasing to 20k ius when sick.

    M

  • Melinda P

    9/13/2011 5:05:38 PM |

    Is taking a high dose of Vitamin D3 during pregnancy safe? I know most of the "recommendations" are to take 200 IU, but I have some 5000 IU pills in my cabinet, and am wondering if those would be safe or not. Or should I find a lower dosage pill?

  • Dr. William Davis

    9/14/2011 2:43:36 AM |

    Hi, Melinda--

    Sadly, there are next to no data for how to best manage vitamin D and pregnancy. However, common sense would suggest that achieving a desirable blood vitamin D level should not be harmful, else getting a tan while pregnancy would be harmful, too.

    A dose of 5000 units typically yields a healthy blood vitamin D level in the majority of females.

  • rose

    9/14/2011 2:44:09 PM |

    Hi Mike & Dr. Davis!

    Can you please tell me, has anything worked for you yet? I too do not like the feeling I get on Vit D3 but I am only at 31 and need  to start taking 8,000 a day as well.

    Also Doctor Davis can you please please elaborate on these: "parathyroid and adrenal status, e.g., PTH, calcium, and salivary cortisols". and why they would booby trap the Vit D3 efforts? How does someone work around this ang take Vit D3?? I found out yesterday I happen to have a high Reverse T3 and need to go on thyroid meds and also have adrenal issues. As well as low insulin levels. So I might be the one who is getting booby trapped.

    Any help appreciated

    Thank you!

  • rose

    9/14/2011 2:46:23 PM |

    Hi Mike & Dr. Davis!

    Doctor Davis can you please please elaborate on these: "parathyroid and adrenal status, e.g., PTH, calcium, and salivary cortisols". and why they would booby trap the Vit D3 efforts? How does someone work around this ang take Vit D3?? I found out yesterday I happen to have a high Reverse T3 and need to go on thyroid meds and also have adrenal issues. As well as low insulin levels. So I might be the one who is getting booby trapped.
    My Vit D3 is only at 31 and have been prescribed 10,000  a day. I really want to start but I have not liked how I have felt in the past on Vit D3.
    Any help appreciated

    Thank you!

  • Dr. William Davis

    9/15/2011 11:49:44 AM |

    Hi, Rose--

    The key here is to find someone who can guide you along while monitoring and interpreting these factors. The greatest difficulty: finding a healthcare practitioner with the knowledge, experience, and interest in doing so.

    As crude as it is, you are still best with word of mouth: asking friends and family who has been a helpful advocate with health problems, especially those involving vitamin D.

  • Reikime

    9/22/2011 2:40:34 AM |

    Hi Dr. D,
    I posted a question on another thread about vitamin D and calcium levels and now I think this thread is more current and probably relevant .
    I am being worked up at the moment for a possible parathyroid adenoma. My serum calcium has been trending up for the past few years and is now 10.3 (x2).
      Way back in 2005 I started reading about the benefits of supplementing with D and used 1000iu/day, as well as 400-800 magnesium and Life Extension's K2. Fast forward to 2009 and imagine my surprise at my D levels being 26!  Increased it to 5-6k per day and went to 43.
    Dr. James Norman is considered to be the foremost expert on all things parathyroid here in the US , and his website : parathyroid.com.  was very informative for me, but concerned me regarding blanket supplementation of vitamin D.
    I respect your opinions greatly and would like your thoughts as to his information.

    Thanks!
    Reikime (RN)

  • Dr. William Davis

    9/23/2011 12:46:10 AM |

    Hi, Reikime--

    I am obviously no authority on parathyroid tumors. Dr. Norman's website is very interesting and makes great sense. I, too, in looking at vitamin D, calcium, and PTH levels have uncovered several parathyroid tumors. It appears to be a lot more common than previously thought.

    The only issue I would disagree strongly with is the statement that the ONLY purpose of vitamin D is to increase intestinal absorption of calcium. In fact, among the most exciting areas of research with vitamin D are a new appreciation for the widespread, multi-faceted effects vit D has in multiple, perhaps all, organ systems.

  • Johnny Bourdeaux

    9/28/2011 2:39:58 AM |

    Hi Dr Davis,
    It seems that a finnish University is doing a major study on Vitamin D, check this out!

    "The FIND will be a randomized, double-blind, placebo-controlled, 5-y supplementation study of the benefits and risks of vitamin D in the primary prevention of CVD and cancer among 18000 men ≥60 y and women ≥65 y. The participants will be randomized to 3 groups with 6000 in each, with daily supplementation of either: 1) 40 µg/d (1600 IU) of vitamin D3, 2) 80 µg/d (3200 IU) of vitamin D3, or 3) placebo. Compliance, use of non-study drugs or supplements, diet, development of endpoints, and CVD and cancer risk factors will be assessed by questionnaires. Blood samples will be collected for assessment of effect modification by baseline 25-hydroxyvitamin D, as well as for future ancillary studies of genetic/biochemical hypotheses."

    https://www.uef.fi/nutritionepidemiologists/find2

    Looks awesome to me. What do you think? Highest dose arm 80 µg a day for 5 years is more than VITAL.

  • Dr. William Davis

    9/29/2011 1:04:13 AM |

    Hi, Johnny--

    Excellent!

    In the meantime, the effects I continue to witness are so powerful that I still advocate correcting vitamin D to 60-70 ng/ml.

  • N

    11/30/2011 6:51:30 PM |

    Hi Doc,

    A quick question on vitamin D:
    I recently tested at 17 ng/ml for vit d.  (had been supplementing w/ 2000 iu of D3 for 2 weeks previous to that).
    The doc is recommending I take 40,000 IU once a week for several months until it stabilizes, and then switching to lower supplementation.

    A few questions:
    (1)  Obviously this will be D2 not D3 since it's prescribed - just go with it?  I believe I read a study somewhere that showed D2 ended up being as effective as D3 despite being slower.
    (2)  Thoughts on taking these large "catchup" doses rather than a more consistent 10,000 IU/day regimen?

    My other stats:  Age 31, 160lbs, Total Cholesterol = 204, HDL = 60, Triglycerides around 100.

  • Dr. William Davis

    12/1/2011 4:20:49 AM |

    You are closer to the truth, N, than your doctor. Clearly your doctor is fairly ignorant of the emerging issues with vitamin D.

    While dosing can vary, depending on body size, race, genetics, etc., 10,000 units per day of D3 would be a typical effective dose.

  • Lynn Ertell

    12/16/2012 6:40:56 AM |

    I had read that about 20-30 minutes of sunlight daily were required for Vitamin D absorption.    Having already gone through Mohs surgery for a tiny basal cell carcinoma on my nose - and being "melanin challenged" - I have always tried to cover up or stay out of direct sun.  Sun blocks apparently have some questionable compounds in them.  I jog 2 miles every day if its not raining or snowing.  So on a sunny day that's 20-30 minutes of exposure.  Should Vitamin D dosage be varied according to daily sun exposure ?   Self-prescribing dosage of supplements is a real headache for me.  I don't have a clue.   It would sure help if there were affordable food sources of sufficient Vitamin D.   What about dairy ?

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