Can protein turn into fat?

I've had a lot of questions and comments about dietary protein and what happens to it, particularly when one is on "zero carbs". Here are some thoughts:

1) If your body is in glucose deficit and you are not getting enough dietary glucose, then gluconeogenesis will supply the glucose. Short term deficits, however, are met by making glucose from the glycogen in your liver, not by breaking down proteins. A simple fall in serum BG does not crank up the GNG machinery. GNG happens to replenish your glycogen, not after a single weight lifting session, just if there are no carbs by your next meal and your liver glycogen has been run down too far.

2) If glycogen stores are depleted and need to be rebuilt, they will be replenished from dietary glucose first. If there is not enough dietary glucose, dietary protein will be used (60% or 70% conversion ratio, pretty close) next. If there is not enough dietary protein (amino acids actually) then existing structural proteins in your body will be used to supply the amino acid feedstock for GNG to make the necessary glucose. Please remember that what is really happening is that proteins are constantly turning over into AAs in your body all the time. If you are deficient in dietary protein (no protein bolus at the next meal) , they are broken down and then are not being re-built. You are not directly scavenging your muscles, you are just failing to re-build them. Proteins and even fats are not static. Gaining or losing muscle or storage fat is a dynamic equilibrium process controlled by hormones, etc.

3) Protein eaten in excess of structural and enzymatic (our enzymes are proteins) needs, and in excess of GNG requirements if you eat no carbohydrates, can be burned as fuel for energy. This is why we say that protein has a caloric value of about 4 kcal/g, just like glucose. If it is burned as fuel, that is the energy density. There is no " every gram of protein turns into such and such" It depends on many variables.

4) Any macronutrient with caloric value (carb, protein or fat) can be burned for fuel. Any of these can also be stored as fat if they are in excess. Note I said, "can be" stored as fat. Insulin is the nexus of processes that end in fat storage. If insulin levels are lowered from your previous baseline, fat storage is inhibited (remember the equiibrium?) so you tend to lose fat down to a new equilibrium. You will tend to stay at that new equilibrium based on in my opinion, two things: spontaneously lower caloric intake and possible increased wastage or burning of any excess caloric value. (See your bible: GCBC by Gary Taubes)

The reason dietary proteins are less likely than carbs to end up as fat is the same reason dietary fat on VLC is less likely to end up as fat. It is not because they can't be converted to fat. Of course they can! It is because eating fat and protein and very little carbs keeps your insulin levels low, get it?

Once again, macronutrients influence hormones, and it's the hormones that direct fat storage.

Think how food affects hormones, not whether this or that food component "turns into fat".

Food only turns into fat at the direction of hormones.

Hormone levels (AUC or area under the curve) can be stable within a range of different macronutrient ratios. Your insulin levels in particular only drop so far. That is why I say repeatedly it is not biologically plausible that most people need to tightly define their macronutrient ratios, anymore than it is biologically plausible that you need to use a scale and a calculator to regulate your weight. 

Like natural gas, oil and coal in the industrial environment, carbs fats and proteins have specific structural uses in our bodily environment, but each has a potential value (not required, but potential) as fuel to keep the metabolic fires burning. Natural gas is both a feedstock to make plastics and a fuel that can be burned. Oil can be used to coat your driveway or turned into gasoline for your car.

There is not any "typical" thing that always happens to a molecule of glucose, fat or protein. It depends on what the body needs.

As far as raising your insulin levels, glucose has the biggest effect, and fructose is bad because it induces insulin resistance, which requires you to produce higher levels of insulin to handle the same amount of glucose. Protein requires insulin but less than glucose and there is some insulin response to dietary protein. There is no insulin response to dietary fat. All three require some basal insulin for normal metabolism.

How much sun?

Prompted by a reader question, here are some brief thoughts on how to get your Vitamin D the natural way.

I have seen old photos of native americans and Inuit - some of them look pretty wrinkly. I have seen photos of very old black africans and some darker skinned asians (Thai) who have skin that looks very smooth despite their age and lots of sun exposure. I have seen images of caucasian surfers in California and Hawaii who are deeply tanned but look pretty wrinkle free for their age. The most wrinkled people I see where I live get little sun and eat the SAD.

There are certainly genetic factors, including skin type.

I am doing some speculation with an evolutionary bias here, but here is my working hypothesis.

If you are a light skinned white, your melanin is low specifically to allow you to gather UVB to create D. It is not logical that this trait evolved and came with the side effect that the amount of sun required to maximize your D exposure also ruins your skin. I think that PUFAs and inadequate immune and cellular repair mechanisms and smoking themselves create skin damage and potentiate any UV damage that occurs. I think any person should be able to tolerate whole body sun exposure up to the point right before burning, whether that is 15 minutes or 8 hours depends on skin type. This will also be the amount that optimizes vitamin D.

If you are white and you go hours beyond burning every day, you may be damaging your skin beyond repair capacity and may hence be causing premature aging.

If you are black and only get 20 minutes a day you will cause no damage but will be D deficient.

So, a white person with type 3 skin, proper diet and spending an hour a day in the nothern sun in summer - no premature aging - plenty of D (If levels are low, could probably tolerate more sun)

Same person living in san diego and gettiing 6 hours a day surfing - maybe some sun damage - more than smoking or PUFAs ? I don't know.

Black skin in the north - naked all day with no premature damage -may still not get enough D

Black skin at the equator -no problem with plenty of D

Any dermatology study you read the subjects will be on the SAD. My minimal erythemal dose has at least doubled (not counting the tanning) since eliminating excess O6s.

Bottom line to my hypothesis: tolerable sun exposure for your skin type should be roughly the same as what optimizes your Vit D levels. Beyond that may age your skin prematurely.

Raw Paleo and Zero Carb - right for the wrong reasons

Since the site seems to be attracting some interest from the raw crowd, I'm going to tell you what I think of the raw idea.

Much of the raw paleo discussion emphasizes the raw over the paleo. Raw modern fruit loaded with fructose is more paleo than lightly cooked meat? Not a chance.

Whether a food has been subjected to heat is more important than the macronutrients, micronutrients and antinutrients in the food? That seems absurd as an organizing principle.

We have not had time to metabolically adapt to cooking? Whether we have been eating cooked food for merely 250,000 years or millions as Richard Wrangham claims, there has been plenty of time for us to adapt to cooking. I don't find any of the arguments against cooked food convincing.

Where does the raw is better idea even come from? It seems based on analogical or simple syllogistic reasoning rather than science. It takes technology to cook, so we must be better off without cooking because other animals can't cook? There is very good evidence humans evolved in a divergent fashion from other primates. As gorillas went in the direction of vegetarianism, hominids since H. Habilis over 2 M years ago evolved to eating other animals. I believe the caloric density and efficiency of becoming predators and exploiting the fat stores of other animals allowed developmental energy to be devoted to brain growth, which in a virtuous cycle, allowed development of social organization and technology including organized hunting coordinated with gathering and cooking technology. This social and technological evolution combined with carnivory fed back into further brain growth in a positive feedback loop over (at least) hundreds of thousands of years culminating in H Sapiens.

But let's say I am wrong and cooking is only 50,000 years old. Even if that were so, where is the evidence in the present that we are not adapted to it? Unlike the case with wheat, linoleic acid and fructose, I've seen no medical evidence cooking is bad. The PaNu method is informed by science. To posit evolutionary discordance requires harm in the present, not just lack of evidence we did it back in the day.

How about refrigeration? That is less than 100 years old. I wonder how many raw paleo folks refrigerate their meat? Shall we shun refrigerators because only fresh or rotten meat is truly "paleolithic"? I say only if there is some biologically plausible medical reason to suspect refrigeration (or central heat, or laptop computers, etc..) is bad for us.

PaNu is about metabolism, not food re-enactment. Simple analogical reasoning without attempts at falsification can easily lead to the same silly emotional reasoning used by vegans like Ingrid Newkirk (a rat is a pig is a dog is a boy...)

Raw paleo is based on a completely unsupported dogma against cooking that has zero basis in biochemistry, medical science or paleoanthropology. It is based on weak analogical argument only. Positing that the core dogma is that everything should be raw and then arguing over a spectrum from raw veganism to 100% meat ignores the most fundamental elements of metabolism. Saying that butter or cream are not "paleo" because they were not consumed way back when, when these animal based sources are nearly pure animal fat is just nonsensical.

The good news is raw paleo seems to exclude wheat, non-fruit sugar and excess plant oils. I like where most of raw paleo ends up, I just don't like how they get there.

As far as the "zero carb" thing, I have the same concerns. Saying all carbs are bad, and we cannot tolerate them at all is just another unsupported dogma. Saying we don't need carbs vs making a fetish of totally avoiding them can lead you to very different places, one of which is the reasonable accusation of being cultish and unscientific - this impedes spreading the message and hence makes it harder to help non-fanatics with their health. My own diet is nearly zero carb some days but I have never claimed that that is is better than 10 or even 20% carbs. I am not saying it is not, I just don't have evidence that it is.

I eat my meat so rare it is almost raw and I eat sashimi and tuna completely raw. But not because of raw dogma, I just like it that way. I eat no potatoes or white rice or yams because I am sensitive to starch, not because I have unequivocal evidence they are bad in small quantities. I eat a VLC nearly carnivorous diet. The most important elements of this are no wheat or other grains, zero plant oils and very low fructose. Whether the carb level is 2% or 10% or even 20% with preservation of these more important parameters, I have not seen evidence there is a difference.

PaNu is often conjectural, but will always be based on science and I am constantly looking for evidence I might be wrong.

PaNu is proscriptive (don't eat that food!) because the way to the EM2 is to avoid the neolithic agents of wheat, linoleic acid and fructose, not through duplicating a particular dietary composition from the paleolithic period - there was too much variety to even do that, and much of what I read about what paleo man ate is pure conjecture if not paleofantasy.

I am fairly confident about what paleo man did not eat, however, and that makes our task much easier.

I welcome zero carbers and raw meat carnivores - you are way healthier than those on the SAD, but your will is more durable if backed by a resilient science instead of a rigid and brittle faith.

Vitamin D

First let me thank you all for your patience in waiting for this post and for your interest in the blog. I’ve lately been  a bit busy with my day job. I also have duties managing various investments and being the building maintenance and IT guy for my wife’s dental practice, so there may be slow periods from time to time as a result.

You have no doubt also noticed that this is, so far, not one of those “here is what I ate today” blogs. Nothing wrong with that - I have a good camera - it’s just not my focus. The ratio of background reading and research per post is usually high and likely to stay that way.

I am very gratified by the positive response to the site. I first began this as a resource for patients and friends only 2 months ago. I don’t have one of those page-counter-gadgets displayed but the site has had over 7,000 unique visitors and about 35,000 page hits in that time. Your interest and intelligent questions help motivate me to learn more and keep blogging, so thank you all for that.

On to the topic.

Vitamin D is a prohormone or hormone precursor and not really a vitamin. Like cortisol and the sex hormones estrogen and testosterone, it is derived from cholesterol molecules. It is technically a secosteroid, as it is derived from cholesterol with the “3’ ring broken open.

Vitamin D is phylogenetically old, being found in simple organisms that have been around for as long as 700 million years. A molecule being preserved through that much evolutionary time is usually a clue that it could be important. Ultraviolet light (UV) is part of the spectrum of solar irradiation that has bathed the earth since before life began. (Before the air was poisoned by oxygen and the ozone layer formed, there was much more incident UV than now.) Vitamin D2 (ergocalciferol) is the more ancient plant and fungal version of D and is formed from cholesterol with UV light. D2 may have originally evolved as a kind of sunscreen in these simpler organisms. Animals evolved a chemically different form of D, called D3, which is formed via UV light and 7-dehydrocholesterol. Animals with feathers or fur create D3 photochemically within the oils on their feathers or fur, and then lick themselves to get their dose of D. Humans make D3 in the bottom two layers of their epidermis in a photochemical reaction driven by UV in a narrow band centered on about 297 nanometers wavelength – known as UVB. This opens the 3 ring in 7-dehydocholesterol and there follows a quick thermally driven isomerization:

This results in vitamin D3 or cholecalciferol, which goes to the liver and is converted to 25-hydroxycholeclaciferol or 25 (OH) D. 25 (OH)D is what we are most interested in clinically and nutritionally. It is the blood and tissue levels of 25 (OH) D that determine your Vit D status. 25 (OH) D is fat soluble and stored in adipose tissue and clinically these fat stores of D have a half life of about 2 months so it takes a few months of darkness to get deficient if you start out healthy, but it would be hard to still be stoked up after 6 months of a Wisconsin winter. When you replace D orally, you are usually taking D3 as Cholecalciferol – it is absorbed in the gut and carried into the blood in chylomicrons, makes its way to the liver and is then converted to 25 (OH)D. 

The much more high-potency active form of Vit D has an extra hydroxyl group and is 1,25 (OH)D or calcitriol. Calcitriol is found in concentrations about 1000 times lower than 25 (OH) D in the serum. This is important as although 25 (OH)D has some end-organ effects, including on its own synthesis, the major hormonally active D is calcitriol. The kidney is one primary end organ mediating the classical effects of Vit D and it is here that 25 (OH)D is converted to calcitriol like this:

This calcitriol made in the kidney then circulates and acts on the classical target organs of the gut, the bones and the kidney itself. The effects on these organs center around calcium ion homeostasis. Calcium levels must be tightly controlled for proper cell functioning, so it is no surprise that calcitriol levels are tightly controlled regardless of 25 (OH)D levels. One can therefore be 25 (OH)D deficient and have normal serum calcitriol levels. That is why you must measure 25 (OH)D to assess Vitamin D status and not calcitriol. 25(OH)D in the serum is in equilibrium with tissue stores of 25 (OH)D and these levels are the ones that determine health or deficiency.

Classical effects of Vitamin D

The classical effects of Vitamin D are the ones I was taught in medical school. They have been known for the longest and are well understood. The focus is on maintaining appropriate calcium levels, as multicellullar animals that have circulatory systems need a calcium ion concentration that is fairly constant, regardless of eating schedules, hydration status, etc., in order for cells to work properly. Vitamin D and parathyroid hormone (PTH, secreted by 4 or so ridiculously tiny glands behind the thyroid gland in your neck) work in concert to balance calcium absorption in the gut, filtration of calcium and phosphorus at the kidney, and turnover of hydroxyapatite in bone. Hydroxyapatite composed of calcium and phosphorus is the “concrete” of your bones, providing compressive strength. You can think of the collagen matrix in your bones as the “steel rebar”, providing tensile strength and elasticity. A tired metaphor, but it works for me.

Your body emphasizes staying alive first, so bone strength is secondary to calcium homeostasis when push comes to shove. You could say that when calcium is short in the bloodstream, PTH will view your endoskeleton as a big reservoir containing 1 kg of calcium. When you are a Paleolithic human, with minimal clothing and forced to spend time outside foraging, your D levels and calcium levels are concordant with the way the EM2 has selected us to function. When you are a Neolithic human (like, say, a radiologist working in a windowless room and living at 45 degrees north!) your 25(OH)D levels are suddenly chronically artificially low, and hey, not my design, but now you are absorbing 15% of your dietary calcium instead of 70%, and you are peeing out more in your urine. Your serum calcium levels come before your bone strength, so now PTH (in one of it’s actions) increases and acts to encourage specialized bone cells called osteoclasts to literally start dismantling the hydroxyapatite “concrete” in your bones in order to supply your blood with calcium.

Rickets and Osteomalacia

So if you are a Neolithic human that has just been weaned, and you live in the late nineteenth century in London, which is not only far north but has what little sun is there being screened by soot, your growing skeleton may be affected by Rickets – severe hypovitaminosis D in the skeletally immature- and you may end up bow-legged or knock-kneed. If you are an adult with a mature skeleton, there will not be the same deformity, but you may have osteomalacia  - collagan matrix “rebar” is laid down but there is inadequate hydroxyapatite “concrete”. This can have a painful periostitis in addition to weakening of the bone.

Osteoporosis

Osteoporosis means lower than desirable bone density with increased fracture risk and is a condition endemic in older folks on a Neolithic diet. It is different from osteomalacia in that the ratio of collagen matrix “rebar” to hyroxyapatite “concrete” is correct, but the total bone mass and density is low. Neolithic osteoporosis is probably multifactorial, in my opinion mostly caused by excess grain consumption, inadequate consumption of animal products in general and animal fats in particular, and is likely most related to low vitamin D and low Vitamin K2. When the D deficiency is severe, there is secondary hyperparathyroidism and PTH is measurably elevated in response to low calcium levels. Vitamin K2, especially Menaquinone or M4, is a cofactor for osteocalcin (which helps make bone) and Matrix Gla protein (which helps remodel or remove it). Please see Stephan’s fascinating posts on the importance of K2 for proper maxillofacial development, bone and dental health and cardiovascular health. K2 is also important to blood clotting and also seems to be part of the atherosclerosis puzzle – it helps to prevent atherosclerotic vascular calcification and some animal studies suggest it may reverse vascular calcifications. So K2 is needed both to make bone and to remove bony or bone-like calcifications.

For osteoporosis treatment, trials in Japan suggest K2 supplementation is highly efficacious, with one trial showing 80% reduction in hip fractures with K2 supplementation. This is much more impressive than the rather modest improvements in fracture risk reported so far with Vitamin D supplementation, but to be fair, the doses used with D have been very small, in the 400 -800 iu/day range. More on doses later. Calcium supplements seem to be the least helpful for osteoporosis, which makes sense when you understand that absorption from the gut can be very poor without D and very high with adequate D levels. It is not logical that we should need calcium as a supplement at all as long as D3 and K2 are at Paleolithic levels and you are not binding up dietary calcium with phytates in cereal grains. (Yeah, I know, you can soak the grains overnight, but that does nothing to the gliadin proteins and wheat germ agglutinin. Exactly how many reasons do you need to not eat grains?)

Vitamin D receptors (see below) are also found on skeletal muscle cells. Many fractures in the elderly may be related to muscle weakness contributing to more falls. It is speculated that in addition to age-related sarcopenia (loss of muscle mass with age) causing muscle weakness, there may be muscle weakness from lack of Vitamin D to properly stimulate muscle cells.

Vitamin D, grain avoidance and eating grass-fed butter and hard cheeses (for the K2) are my strong recommendations for avoiding osteoporosis. I doubt if bisphosphonate drugs work better, and there is no way they are safer than butter.

Non-classical effects of Vitamin D 

It seems that this hormone does much more that “just” regulate calcium ion homeostatis. The vitamin D receptor, or VDR, is a nuclear receptor. Nuclear receptors are found within the cell, sometimes on the nucleus itself, and are bound by the signaling hormone when it enters the cell. The hormone-receptor complex attaches to a specific site adjacent to the location of a gene on your DNA inside the nucleus, inducing the DNA to be “read” and transcribed into a protein. The gene turned on and the protein produced will be specific to the cell type and this explains how a single hormone can cause mutiple effects in the body depending on the type of cell having the receptor.

In the case of Vitamin D, there are VDRs found in many cells besides the Kidney, small intestine, bone cells and parathyroid gland we discussed above.

Immune function

VDRs are found on B and T lymphocytes and monocytes, all cells involved in immune function. D3’s effect on immune function improves resistance to infection by strengthening the innate immune system, for instance by supporting phagocytosis and destruction of invading organisms. D3 also modulates the adaptive immune response to better differentiate self from non-self. This latter effect, modulation of the adaptive immune response, appears to be involved in the ability of Vitamin D to decrease susceptibility to serious and common autoimmune disorders like Type I diabetes, rheumatoid arthritis and multiple sclerosis. Now, this does not mean these diseases are caused by hypovitaminosis D. In fact, Peter discusses how these are Neolithic diseases of molecular mimicry caused by other elements of Neolithic nutrition, namely interaction of a leaky gut from gluten grains and overgrowth of commensal organisms in our guts caused by starches and fiber in amounts that are not optimal. For now, you can search these diseases on Peter’s blog to learn more. I will post more of my thoughts on this phenomenon later.

I view Vitamin D deficiency as just one more Neolithic discordance with the EM2 that increases the likelihood of these autoimmune diseases of civilization, not as the primary cause.

Other elements of PaNu will interact synergistically with restoring Vitamin D to Paleolithic levels, including moderation of insulin levels and correction of the 6:3 ratio. All will conspire to improve immune function, both in terms of improving resistance to infection, decreasing promotion of common cancers, and reducing inappropriate immune responses directed against self-proteins (autoimmune diseases).

Cancer

In addition to immune cells that may control cancer promotion, cells of tissues susceptible to cancer also express the VDR. Vitamin D binds to the VDR and new proteins are synthesized that control cell differentiation, proliferation and recognition of adjacent cells, all functions important in the development of cancer.

The evidence that hypovitaminosis D causes cancer is mostly epidemiologic, but is powerfully suggestive, and unlike, say, the diet/heart hypothesis (cholesterol or saturated fat causing heart disease), has the virtue of biological plausibility and support by laboratory science. The evidence can be summarized thusly:

A wealth of studies show that exposure to UV light (latitude) and in some cases vitamin D intake or serum levels, are inversely related to the risk of common cancers, including colon, breast, prostate, esophagus and non-Hodgkin lymphoma. African Americans are particularly likely to be D deficient and have higher rates of many cancers, especially when they live at higher latitudes. The same latitude epidemiology supports the effect of D on risk of MS diabetes and hypertension.  One review suggested that supplementation with 1000 iu/day D3 would decrease colon cancer by as much as 50%. There is evidence both for reduced incidence (risk of getting cancer) and reduced mortality if you get it. Making sure my Vitamin D levels were high is the first thing I would do if I were diagnosed with cancer. 

A trial from Creighton University investigating calcium and Vitamin D at 1100 iu/day for fracture prevention “accidentally” showed 60% lower cancer risk in women over a 4 year period.

Other Effects

Vitamin D replacement improves insulin sensitivity, beta cell function (ability to secrete insulin) and hypertension. Interestingly, these are all effects that counter elements of metabolic syndrome. Vitamin D can be thought of as an anti-metabolic syndrome hormone. How much of Neolithic disease is due to hypovitaminosis D? It certainly seems to be an element. My suspicion is that, like fructose avoidance and maybe lack of excess linoleic acid, high D levels may be one of those things that increase our tolerance for carbohydrates – think of the Kitavans with their high carbohydrate diet but no evidence of metabolic syndrome and preserved glucose homeostasis.

Replacement, Not Supplementation

OK, so now I sound like all the other bloggers. I don’t really believe in supplementation, but......

I have talked previously about my view of the distinction between supplementation, compensatory supplementation and replacement. Supplementation is the belief that there is something magic that was not present in Paleolithic life that can give us “supranormal” health. The belief in dietary antioxidants or novel drugs or eating lots of some unusual particular food is supplementation. It is generally not biologically plausible that there is some completely novel element that can improve health. 

What are the sources of Vitamin D? Even in the deficient population, 80% or more of serum 25(OH)D is attributable to sunlight. Sunlight is effectively the only natural source of significance. You can get some D from fish, beef liver, irradiated mushrooms (D2), etc. Once you are taking cod liver oil (over 1000 iu./15 ml), which is hardly a consistent Paleolithic source, you are replacing at dietary levels which are artificial.

As a source of Vitamin D3, whole body UV between 10 am and 1 pm for 20 minutes will give a D3 equivalent to oral dosing with 10,000 iu vitamin D3 (cholecalciferol). This is a rough estimate - it assumes you are outside only between March and October if north of 37 degrees latitude, and that you are unclothed and have average skin pigmentation where your minimal erythemal dose (MED) is 20 minutes. Black persons may need 5-6 times the exposure for the same dose. There is simply no natural food source that can compare to sunlight.

How much do you need and what is deficient?

Referencing the classical effects of D we might define insufficiency at less than 20 ng/ml and severe deficiency at 10 ng/ml. Current RDAs of 400 iu/day are based on avoiding rickets and were made before there was recognition of the other important effects of D. The dose-response curve for serum levels is highly non-linear, with each 5 ng/ml increment in serum levels requiring a larger increase in daily intake. Even 400 iu/day has been shown to be ineffective in treating osteoporosis. The non-classical effects of D seem to require larger levels to ensure health. Using a few facts we can come up with a more modern recommendation that is safe and reflects a more complete understanding of the importance of vitamin D.

1)   The level of 25(OH)D at which most dietary calcium intake is adequate (absorption is maximized) is 50 ng/ml

2)   The level of 25(OH)D that optimizes fracture prevention is about 40 ng/ml

3)   The level that causes PTH levels to plateau at a minimum (ensures no secondary hyperparathyroidism) is 40 ng/ml

4)   The level of oral D3 intake required to ensure a level of 40 ng/ml in most people is 4000 iu/day

5)   The highest reported level of oral intake that has never been associated with a case of hypercalcemia due to hypervitaminosis D is 10,000 iu/day

NOTE: The following section has been updated as of February 2011

Using the above numbers most of us who are not lifeguards would have D3 insufficiency, if not deficiency by the end of winter. I find that implausible and despite the epidemiology I believe megadosing with Vit D orally is unproven and unnatural.

I think it is reasonable to get some sun exposure up to but not exceeding the minimal erythemal doseIf you can get adequate sunlight at midday, say, sitting outside at lunchtime with 25% of your skin exposed for a half hourr, and your latitude and the season allow enough UV, you can use that as your source. Am I concerned about skin cancer or wrinkles? I think some sunning without burning is fine. I suspect what really trashes your skin are PUFAs and cigarettes, not the sun. If you worry about wrinkling, wear a broad-brimmed hat and get the sun on your arms and shoulders. 

Finally, don’t forget plenty of grass-fed butter or hard cheeses to get your K2.

NOTE: My standard disclaimer that this is not individualized medical advice applies here, only more so. If you take warfarin or other medications, or are otherwise not healthy, always consult your personal physician before taking any drug or dietary supplement.

References:

Vieth review AJCN

Garland review AJPH

Holick review AJCN

Holick and Chen Review AJCN

Willett fracture review JAMA

Rovner Review Archpediatrics

Cockayne Vit K and Fractures

Endocrine physiology Porterfield and White

Calorie Restriction: partial restoration, not enhancement

Zen Teacher Shunryu Suzuki

My previous two posts, here and here, were a two-part explication of the recent paper in Science claiming life extension and mitigation of aging related diseases with calorie restriction (CR) in a rhesus monkey model.

Many commenters and bloggers have been critical of the suboptimal diets fed to the monkeys, and some have therefore questioned the relevance of this study. First let me defend the researchers a bit. The study was begun in 1989, and no doubt was conceived and planned some time before that. The late 1980's were almost a decade before most people had internet access, and it would be fair to say the reigning dietary paradigm, including Ancel Keyes' diet-heart hypothesis, was not being seriously challenged by many. I think a certain amount of cultural relativism is appropriate. I for one was only two years out of medical school. Expressing the idea that corn oil, wheat or sucrose could be poisons might well have threatened my nascent medical career, had I been smart enough to think such thoughts! So perhaps the Wisconsin team can be forgiven for using what was probably considered a very healthy monkey diet at the time. Once committed, they could not very well change it and start over with new monkeys after 18 years of effort because they just read Good Calories, Bad Calories.

That said, I do not disagree with the observation that the control diet was suboptimal. PaNu theory is that there is such a thing as an evolutionary metabolic milieu (EM2) that optimizes our phenotypic expression. That internal metabolic and hormonal milieu is probably quite similar for many mammalian species, but likely differs importantly in food inputs by species, depending on features of the original food econiche. I believe the EM2 of rhesus monkeys is not achieved by massive amounts of corn oil and excess and highly bioavailable sucrose, and many commenters have said the same.

With these flawed diets, is the study still relevant to whether life extension via CR is a real phenomenon?

I believe the answer is yes, but only because it allows us to re-frame the problem with a new question.

That question is: If CR works, what is CR?

This study speaks to the very concept of CR and its ontology as a phenomenon.

If we define CR as the phenomenon of improved lifespan or slower degeneration as a result of lower caloric intake, we can conceive of CR in one of two ways:

1) We have discovered a phenomenon that takes our natural aging phenotype and attenuates the aging process - an enhancement of our phenotypic potential

2) CR is a phenomenon that represents one of several ways that the damaging effects of our neolithic diets can be mitigated, and is likely mediated through lowering basal insulin levels. The CR effect is one among many changes to the neolithic diet that could be made, and which, if they work, are not enhancing our natural aging phenotype, but rather restoring it. Any such maneuvers will work only to the degree we were deviating from the EM2 for our species in the first place.

Listless and anorexic folks on plant-based diets, and those searching for profitable chemicals to sell us are promoting idea #1.

PaNu favors #2.

To the degree that CR or any dietary maneuver works, it is just getting us fractionally closer to the EM2 for our species. I believe the EM2 can be achieved or closely simulated with an ad libitum low carbohydrate diet relying on animal sources that minimizes fructose, gluten grains and linoleic acid. Accordingly, it is unlikely that any drug, intervention, or supplement can ever improve on what can be achieved with diet alone. From what I know so far, I believe the laboratory experiments with mammalian species to date can be interpreted this way. If the model animal lives longer, you are just mitigating the effects of an artificially unhealthy diet.

CR is therefore just a partial restoration of our optimal phenotypic expression, not an enhancement of some "natural" state.

I guess this is a little like the Soto Zen concept that you do not need to seek enlightenment because you are already enlightened. Enlightenment (Health) is not something outside yourself you can acquire from some special experience (medical science), but rather a potential you have always carried within you.

CR as practiced by Humans on plant-based diets is probably lowering basal insulin levels in the unhealthiest of several possible ways.

The healthiest and most sustainable way would be an animal-based low carbohydrate diet that minimizes wheat, fructose and linoleic acid.