IMPORTANT! YOU MUST READ THIS BEFORE CONTINUING:
by Ron Brown, Ph.D., author of The Body Fat Guide
THE CAUSE OF male pattern baldness, or androgenic alopecia, is commonly blamed on genetics. If your father or grandfather was bald or had thinning hair, you, as a male offspring, supposedly have an increased risk to suffer a similar fate. Research studies on immigrants, however, suggest otherwise!
Many genetic theories about the cause of ill health have been refuted (proven false) by findings from migrant studies. For example, people who migrate to different countries and change their eating habits may show a rapid and significant increase in the incidence of chronic diseases that are prevalent in their adopted country. Such rapid changes in health cannot be explained by genes alone because genes often require many generations to mutate. A rapid change in male pattern baldness that cannot be explained by genetics alone has been found in several migrant studies.
Researchers reported a high amount of hair loss in people from Turkey, Indonesia, Morocco, and Cape Verde who immigrated to cities in Europe (Graham-Brown et al., 1990). Another study found significant hair loss among European immigrants from North Africa, the Middle East, India, and East Asia (Dalgard et al., 2007). It was Japanese researcher Masumi Inaba who first suggested that a change to a Western diet high in animal fat over-stimulated sebaceous gland secretion and was responsible for increased hair loss in immigrants from Japan to the United States after WWII (Inaba, 1986). But is animal fat really the culprit that causes male pattern baldness? This article attempts to expand upon this explanation with updated research.
If animal fat is the disturbing factor that causes alopecia, then people following a low-fat diet should have less hair loss than people following a low-carb diet that is higher in animal fat; and that's exactly what one random-controlled trial showed (Foster, 2010)! But animal fat is also associated with dietary cholesterol and cardiovascular disease, and researchers have found a link between male pattern baldness and cardiovascular disease (Lotufo, 2000). Is it possible that cholesterol also plays a causative role in alopecia?
For example, testosterone is a hormone associated with androgenic alopecia, which explains why alopecia is a problem seen mainly in mature males. An important clue linking cholesterol and alopecia is that testosterone is biosynthesized from cholesterol. Furthermore, research shows that cooked or oxidized dietary cholesterol is converted to oxysterols that have been shown to absorb into the lining of arteries and cause arterial plaque (See How Cooking Clogs Your Arteries). Is it possible that oxysterols somehow also target the root of the hair follicle as a free radical and damage it, causing oxidative stress and hair loss?
One possible way that oxysterols may come in contact with hair follicles is by being synthesized into testosterone. Perhaps oxysterols may transfer their increased oxidation state to testosterone and give testosterone the proclivity to target scalp hair follicles that it normally does not target, much like a free radical attaches to other molecules to steal electrons. Although all hair follicles on the scalp and body contain receptors for androgens like testosterone, testosterone usually only binds to and stimulates follicles of body hair that grows as a secondary sex characteristic, (Randall & Botchkareva, 2009). The scalp hair follicles may respond to the binding testosterone/free radical as a foreign entity, and initiate an inflammatory and immune response, much as occurs when oxysterols absorb into arteries. It has been observed that oxysterols don't pack properly into the endothelial lining of arteries. Similarly, it may be that the geometric configuration of the testosterone/free racial is altered by oxysterols and does not fit into the follicle receptors properly. Another possibility is that oxysterol uptake in the membrane of the androgen receptor reduces membrane selective permeability, allowing large biomolecules to enter the receptor through transcytosis.
Regardless of the exact mechanism that causes it, research confirms that alopecia is associated with inflammation and an immune response within the hair follicle (Panicker et al., 2012). Just like plaque forms in arteries as part of the inflammatory and immune response, plaque may form in the hair follicle root from secretions of the auxiliary sebaceous gland, and the follicle falls dormant. In the meantime, the testosterone that remains attached to the follicle is converted to dihydrotestosterone, which may be a neutralized end-product of the hair follicle pathology that remains encapsulated by the plaque, rather than causing the pathology as is commonly suspected. If the plaque dislodges, it would then carry away the dihydrotestosterone with it.
Of course, this is just a hypothesis suggesting a possible oxidative stress mechanism for the cause of hair loss. There is also evidence that oxidative stress from hydrogen peroxide, a lipid oxidation product, is associated with hair graying (Wood et al., 2009). Trüeb (2009) summarized: "There is circumstantial evidence that oxidative stress may be a pivotal mechanism contributing to hair graying and hair loss. New insights into the role and prevention of oxidative stress could open new strategies for intervention and reversal of the hair graying process and age-dependent alopecia."
Several questions remain to be explained by the testosterone/free radical hypothesis: For example, why isn't every man who eats a Western diet bald? Actually, up to 70% of men show signs of hair loss by age 70. According to the testosterone/free radical hypothesis, the extent of hair loss depends on the various levels of testosterone manufactured in the gonads of individual men. Anybody who watches televised pharmaceutical commercials for testosterone replacement therapy knows that some men produce less testosterone than others. We also know that eunuchs and other castrated males don't lose their hair!
Also, why are only the scalp follicles on the top of the head affected in alopecia? Perhaps simple gravity prevents the clogged follicles on the top of the scalp from dislodging the accumulated plaque as readily. Standing on one's head would seem to help, but this is probably not necessary for two reasons. One: Unless the cause of the problem from oxidative stress is removed, more plaque will continue to accumulate in the follicles regardless how much one stands on one's head! Two: Assuming gravity exacerbates follicle clogging, reclining during sleep would be sufficient to assist the follicles to unclog naturally when oxidative stress is reduced. Furthermore, lipid packing defects caused by oxysterols in membranes are reduced under higher pressure, and it is possible that the hair follicles that hang off the side of the head are under more pressure due to the force of gravity compared to follicles resting on the top of the head. The pattern of blood circulation in the scalp is another factor that could effect the distribution of oxysterols in cell membranes of the scalp.
What is more important is that research suggests that avoiding dietary cholesterol in animal-based foods and reducing lipid oxidation products by eating more raw natural foods may be the solution to reverse hair loss and hair graying as well as to prevent cardiovascular disease and other chronic diseases. Gary Null, Ph.D., has placed people on plant-based diets containing large amounts of raw natural foods, and he claimed that subjects who were able to complete his program protocol re-grew lost hair and reversed graying! Nathan Pritikin, who avoided lipid oxidation products by eliminating almost all dietary fat (not recommended), and Ann Wigmore, who ate mainly raw food containing no lipid oxidation products, both appeared to retain their natural dark hair color later in life. More research is needed...
Researchers confirmed that the dermal papilla or hair root follicle from a balding scalp contains a higher level of reactive oxygen species or free radicals compared to a normal scalp (Upton et al., 2013).
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