3. Why Does Sulfur Deficiency Lead to Obesity?

To summarize what has been said thus far, (1) foods are becoming depleted in sulfur, and (2) locations with naturally high sulfur deposits enjoy protection against obesity. Now comes the difficult question: why does sulfur deficiency lead to obesity? The answer, like much of biology, is complicated, and part of what I theorize is conjecture.

Sulfur is known as a healing mineral, and a sulfur deficiency often leads to pain and inflammation associated with various muscle and skeletal disorders. Sulfur plays a role in many biological processes, one of which is metabolism. Sulfur is present in insulin, the essential hormone that promotes the utilization of sugar derived from carbohydrates for fuel in muscle and fat cells. However, my extensive literature search has led me to two mysterious molecules found in the blood stream and in many other parts of the body: vitamin D3 sulfate and cholesterol sulfate [Strott2003]. Upon exposure to the sun, the skin synthesizes vitamin D3 sulfate, a form of vitamin D that, unlike unsulfated vitamin D3, is water soluble. As a consequence, it can travel freely in the blood stream rather than being packaged up inside LDL (the so-called "bad" cholesterol) for transport [Axelsona1985]. The form of vitamin D that is present in both human milk [Lakdawala1977] and raw cow's milk [Baulch1982] is vitamin D3 sulfate (pasteurization destroys it in cow's milk, and the milk is then artificially enriched with vitamin D2, an unsulfated plant-derived form of the vitamin).

Cholesterol sulfate is also synthesized in the skin, where it forms a crucial part of the barrier that keeps out harmful bacteria and other microorganisms such as fungi [Strott2003]. Cholesterol sulfate regulates the gene for a protein called profilaggrin, by interacting like a hormone with the nuclear receptor ROR-alpha. Profilaggrin is the precursor to filaggrin, which protects the skin from invasive organisms [Sandilands2009, McGrath2008]. A deficiency in filaggrin is associated with asthma and arthritis. Therefore, cholesterol sulfate plays an important role in protection from asthma and arthritis. This explains why sulfur is a healing agent.

Like vitamin D3 sulfate, cholesterol sulfate is also water-soluble, and it too, unlike cholesterol, does not have to be packaged up inside LDL for delivery to the tissues. By the way, vitamin D3 is synthesized through a couple of simple steps from cholesterol, and its chemical structure is, as a consequence, nearly identical to that of cholesterol.

Here I pose the interesting question: where do vitamin D3 sulfate and cholesterol sulfate go once they are in the blood stream, and what role do they play in the cells? Surprisingly, as far as I can tell, nobody knows. It has been determined that the sulfated form of vitamin D3 is strikingly ineffective for calcium transport, the well-known "primary" role of vitamin D3 [Reeve1981]. However, vitamin D3 clearly has many other positive effects (it seems that more and more are being discovered every day), and these include a role in cancer protection, increased immunity against infectious disease, and protection against heart disease ( Vitamin D Protects against Cancer and Autoimmune Diseases). Researchers don't yet understand how it achieves these benefits, which have been observed empirically but remain unexplained physiologically. However, I strongly suspect it is the sulfated form of the vitamin that instantiates these benefits, and my reasons for this belief will become clearer in a moment.

One very special feature of cholesterol sulfate, as opposed to cholesterol itself, is that it is very agile: due to its polarity it can freely pass through cell membranes almost like a ghost [Rodriguez1995]. This means that cholesterol sulfate can easily enter a fat or muscle cell. I am developing a theory which at its core proposes an essential role for cholesterol sulfate in the metabolism of glucose for fuel by these cells. Below, I will show how cholesterol sulfate may be able to protect fat and muscle cells from damage due to exposure to glucose, a dangerous reducing agent, and to oxygen, a dangerous oxidizing agent. I will further argue that, with insufficient cholesterol sulfate, muscle and fat cells become damaged, and as a consequence become glucose intolerant: unable to process glucose as a fuel. This happens first to muscle cells but eventually to fat cells, as well. Fat cells become storage bins for fats to supply fuel to the muscles, because the muscles are unable to utilize glucose as fuel. Eventually, fat cells also become too disabled to release their stored fats. Fatty tissue then accumulates on the body.