Dukan Diet

Does Dietary Inflammation Reduce Skin Production of Vitamin D?

The media discovered the vitamin D deficiency pandemic last week. Amazingly researchers were recorded on camera saying that the D deficiencies are caused by insufficient exposure to ultraviolet in sunlight and inadequate consumption of vitamin D-laced milk. Have all of these people been avoiding the biomedical journals?

Have they noticed that my tan improved since I started eating anti-inflammatory?

Let’s shine some sunlight on these knowledge deficiencies:

• Serum vitamin D levels have been dropping (as chronic inflammation has been increasing) over the last three decades -- has something changed in our diets?
• Vitamin D deficiencies occur globally (not restricted to Northern latitudes or winter) -- related to diet?
• Women are more vulnerable, because of cultural modesty in some countries, but males are still D-deficient.
• A subset of people exposed to ample sunshine are still D-deficient.
• Vitamin D deficient individuals also have elevated TNF.
• Vitamin D deficiency and inflammation are risk factors in the same diseases.

It seems that the simplest conclusion is that chronic inflammation leads to vitamin D deficiency, even though vitamin D deficiency may also contribute to inflammation.

This also probably means that chronic inflammation makes it harder for skin to produce vitamin D during exposure to sunlight.

One would expect those who are inflamed to get sunburned more readily and people who eat plenty of omega-3 rich seafood probably produce more vitamin D, even if they are not in the sun as much.

Inflammatory starvation (or American fast food) diets high in starch and omega-6 vegetable oils, should produce vitamin D deficiency even on the Equator.

We should not be surprised that inflammatory degenerative diseases are associated with vitamin D deficiency. It would be interesting if vitamin D supplementation to eliminate deficiency, reduced inflammation and reversed degenerative disease.

Do statins reverse vitamin D deficiencies (and improve tanning) as they lower inflammation? [Statin lowering of LDL is unrelated to reduction in cardiovascular disease. Only the anti-inflammatory side-effect is important.]

Does NFkB activation (inflammatory signaling) inhibit vitamin D receptor activity and vice versa?

You can forget all of this confusion, if you just stick with an anti-inflammatory diet (that includes vitamin D supplements) and exercise frequently in the great outdoors.

Miscarriage occurs when inflammation of a pregnant uterus occurs too soon and induces labor. Aspirin, heparin and omega-3 fatty acids lower inflammation and decrease the risk of premature birth.

Pregnancy requires that a woman’s body resist the normal immunological response to foreign, non-self antigens, i.e. the fetus that has half of its genes from the father. This means that conception requires suppression of inflammation and if the woman’s reproductive system has too high a level of chronic inflammation, she may be infertile. In these cases of infertility, suppression of inflammation with aspirin and heparin can permit the woman to become pregnant and sustain a pregnancy to full term. Other approaches, e.g. omega-3 fatty acids and an anti-inflammatory diet and lifestyle, should also be helpful.

Labor and birth are a result of a peak of inflammation as the baby reaches full term. A single aspirin at the first stages of labor can suppress labor. Premature labor can be suppressed with aspirin and heparin, another anti-inflammatory drug more commonly associated with one of its other effects, clot prevention. A recent study showed that omega-3 fatty acids taken as a fish oil supplement were just as effective as aspirin in suppressing premature labor. It may be considered likely that the high incidence of chronic inflammation, prominently recognized in the metabolic syndrome associated with obesity, may significantly contribute to increasing rates of infertility, miscarriage and permature births.

Anti-inflammatory Treatments Cause Inflammation in Some Diseases, e.g. Rosacea

I thought that the anti-inflammatory diet and lifestyle I outlined on this blog would be a general purpose starting point for the treatment of all diseases. Inflammation is the foundation for allergies, autoimmune diseases and cancer. Inflammation is a basic defense against infectious diseases and many tissues require signaling components integral to inflammation for their normal function, so it is possible to overdo anti-inflammatory treatment and produce immuno-suppression. But that is unusual. What I am talking about here is inflammation caused by vitamin D, omega-3 oils, potentially low carbs and inhibitors of NFkB, such as tumeric. This is Paradoxical Inflammation.

Rosacean Inflammation Is Paradoxical

The obvious example of a paradoxical inflammatory disease is rosacea. Rosacea seems to be a large group of diseases that manifest in facial inflammation. Excessive flushing of the face can become persistent and form pustules and swelling. The triggers for rosacean inflammation are legion and idiosyncratic. They include mundane social interactions, numerous foods, temperature extremes and, paradoxically, just about everything that I recommend to decrease chronic inflammation.

Bacteria in Tissue and Gut Biofilms Are Candidates

Why do otherwise anti-inflammatory foods and exercise make rosaceans red in the face? Even vagal stimulation that is uniformly calming to inflammation, can make a rosacean flush. This is very inconvenient. I can only invoke the typical players: cryptic bacteria, biofilms, vagus nerve stimulation and response, lymphocytes/macrophages, cytokines and neurotransmitters.

All rosaceans have demonstrated facial inflammation and have had long term exposure to antibiotics and NSAIDs. That combination suggests that bacteria have been transported from a leaky gut (NSAIDs) to the site of inflammation (the face). It is likely that cryptic bacteria inhabit the dermis near the blood vessels and resident lymphocytes/mast cells. This is also the location for axons from vagus nerves. Thus, vagus stimulation may result in the release of neurotransmitter acetylcholine to stimulate lymphocytes/mast cells with subsequent release of cytokines. In this case the cytokines are inflammatory.

Other sources of inflammatory cytokines are lymphocytes/mast cells activated by endotoxin release from cryptic bacteria triggered by immunological attack. In this case, the immunological attack can be initiated by disruption of the stasis invoked by the cryptic bacteria.

Activated Cryptic Bacteria Are Source of Inflammation

It is hypothesized that the cryptic bacteria remain in tissue, because they are able to induce a hibernation-like physiology in the tissue. Disruption of the hibernation would initiate an immunological assault. Disrupting agents typically include vagal stimulators, such as activators of the hot or cold sensors, e.g. capsaicin, castor oil or menthol. Interestingly, the cryptic bacteria require a residual level of inflammation to acquire nutrients from the host. Anti-inflammatories that inhibit NFkB may destabilize the bacterial/host interaction and result in an immunological attack on the bacteria. All of the attacks on the cryptic bacteria release inflammatory endotoxin.

Gut Biofilms Store Bacteria Recruited to Become Cryptic in Inflamed Tissue

During the course of the disease and following numerous antibacterial treatments, bacteria can be continually recruited from safe havens, such as gut biofilms. Antibiotic treatment of biofilms converts the biofilm community to antibiotic resistance through activated horizontal gene transfer. Moreover, harsh treatment of biofilm communities initiates shedding of bacteria that could migrate across the leaky gut adjacent to the gut biofilms and provide new emigrants into the inflamed face tissue. A likely resident would be Chlamydia pneumonia, which has been demonstrated to be carried by macrophages and offloaded at distant sites of inflammation.

How the Vagus Becomes Inflammatory

This brings up the question of why vagal stimulation shifts from anti-inflammatory to inflammatory in rosaceans. I don’t think that the vagus nerves change in either their activation or in the neurotransmitters that are released as a result of stimulation. This means that the cells that respond to the vagal acetylcholine must be changed. I think that the change is a depletion of Treg cells and the result is that acetylcholine receptors on the remaining T cells cause a release of inflammatory cytokines. These cytokines cause the release of NO by endothelial cells and vasodilation. Leaking of endotoxin from the resident cryptic bacteria causes persistent dilation and restructuring of the vasculature.

Helminth and Il-2 Therapy Reestablish Tolerance and Reverse Vagal Inflammation

Since I have been forced to explain paradoxical inflammatory diseases, I might as well speculate on exotic approaches that already suggest potential treatments. Ingesting parasitic worm eggs (helminth therapy) has proven successful in the treatment of inflammatory diseases such as asthma, allergies and IBDs. Interleukin 2 (Il-2), usually used as a complex with an anti-Il2 antibody, is also a productive treatment. In both of these cases, the treatment stimulates the proliferation of Treg cells, which appear to be deficient in many of the inflammatory diseases. These treatments should also lead to a lowering of inflammation in the gut and suppression of inflammation as a result of vagal stimulation. Inhibitors of acetylcholine receptors, e.g. scopolamine patches, might also be interesting to test to see if they inhibit rosacean flushes in response to typical vagal stimulants such as castor oil or menthol.

Addendum:  Another possibility associated with the heavy use of antibiotics by rosaceans is intestinal (biofilm?) candidiasis.  Yeast infections are common after prolonged antibiotic treatment.  Interestingly, Candida produces resolvins from omega-3 fatty acids and the resolvins suppress neutrophil activity that would attack the yeast.  Thus, many of the anti-inflammatory treatments would actually aggravate yeast infections and contribute to rosacea.  Treatment for candidiasis (keeping in mind that yeast may be protected by biofilms) helps many rosaceans.  Stripping biofilms may be useful if pro- and pre-biotics are used to displace Candida.

Inflammation in response to infection mobilizes the immune system and serves a vital purpose in defense against disease and parasites. Too much or too little inflammation is unhealthy.

A recent report (ref. below) provides a note of caution in the use of anti-inflammatory dietary supplements. Modern diets are inflammatory and provide a major predisposition to degenerative and autoimmune diseases, but the inflammation has some qualified advantages in providing protection to infectious diseases. Densely packed humans survive against the constant threat of epidemics, in part because of heightened dietary inflammation.

The paper listed below shows that habitual use of the potent anti-inflammatory compound in turmeric, curcumin, can effectively lower chronic inflammation. Inhibition of inflammation is not a good thing, however, if the source of inflammation is a chronic parasitic infection of Leishmania. While this article indicates that suppression of inflammation may not be uniformly advised, it does demonstrate the effectiveness of natural products, such as curcumin.

A different study of tuberculosis comparing  land-locked versus genetically related, fish-fed populations, found that the fish eating group was more susceptible to the disease. The interpretation of the results was that the high omega-3 fatty acids of the fish diet reduced chronic inflammation in the coastal community and thereby increased the susceptiblity to TB.

The bottom line for me is that a healthy, anti-inflammatory diet is much safer than the typical modern inflammatory diet of high carbs, high vegetable oils (omega-6), low fruits and vegetables (few antioxidants, low in vitamins C, D and A) and harsh for supportive gut flora. It does leave open the possibility that during an unusual infection a return to fast food may shift your body into a state of high alert.

Adapala N, Chan MM. Long-term use of an anti-inflammatory, curcumin, suppressed type 1 immunity and exacerbated visceral leishmaniasis in a chronic experimental model. Lab Invest. 2008 Sep 15. [Epub ahead of print]