“Prostaglandins, which are produced in the body by oxidizing the polyunsaturated fatty acids, provided an opportunity for the drug industry to get involved in a new market, and the prostaglandins offered a new way of arguing for the nutritional essentiality of linoleic and related acids: A whole system of “hormones” is made from these molecules.”
This should come as a surprise to absolutely no one reading this weblog, but a few weeks ago in a small study found that those suffering from male pattern baldness (MPB) were experiencing heightened levels of an unsaturated fatty acid breakdown product called prostaglandin D2.
For those of you who are not up to speed on fatty acid metabolism, here is a quick primer from my interpretation of Peat's work:
During stress, the cellular need for glucose increases. If glucose requirements cannot be met, adrenaline is released to mobilize glycogen from the liver, and if it’s not there, adrenaline will mobilize free fatty acids for fuel.
Fats are preferentially released from the tissue depending on their saturation. Docosahexaenoic acid (6 double bonds) is released before linoleic acid (2 double bonds) due to the body’s preference for saturated fats to support specific functions.
Normally, the release of fatty acids would create a “negative feedback loop” by inhibiting the release of more adrenaline and cortisol, but because our tissues are dominated by unsaturated fats, the stress reaction is intensified due to numerous factors.
This stressful set of events “turns on” the COX enzymes, which breakdown down these unsaturated fatty acids into “prostaglandins.”
Offensive Lipids
This is where things get controversial.
Prostaglandins are further broken down into three separate groups; series one, series two, and series three.
Mary Enig PhD explains the traditional view of prostaglandins:
“Early research focused on the interplay between the Series 1 and Series 2 prostaglandins. In the simplest terms, the Series 2 prostaglandins seem to be involved in swelling, inflammation, clotting and dilation, while those of the Series 1 group have the opposite effect.”
"The Series 2 prostaglandins do indeed play a role in swelling and inflammation at sites of injury. This is not at all a "bad" effect, but an important protective mechanism—the body's way of immobilizing the affected site to prevent further injury and facilitate healing."
Famously, Peat does not buy into this theory. He believes that the essentiality of "essential fatty acids" has not been proven and that the unsaturated fatty acids, due to their ability to waste oxygen, inhibit glucose utilization (Randle cycle), displace thyroxine and vitamin A from the carrier protein transthyretin, degrade cytochrome oxidase through the displacment of palmitic acid in the lipid cardiolipin, and retard sex hormone binding globulin from removing estrogen—are harmful.
He considers both series of prostaglandins to be, “executors of inflammation” and believes they are misrepresented due to pharmaceutical marketing:
"Prostaglandins, which are produced in the body by oxidizing the polyunsaturated fatty acids, provided an opportunity for the drug industry to get involved in a new market, and the prostaglandins offered a new way of arguing for the nutritional essentiality of linoleic and related acids: A whole system of “hormones” is made from these molecules."
"Since some of the prostaglandins suppress immunity, cause inflammation and promote cancer growth, some people have divided them into the “good prostaglandins” and the “bad prostaglandins.”
Fish Oil Helps With The Pain... Just Like My 5-HTP
On a side note, suggesting that omega-3 is harmful is similar to explaining that excess serotonin doesn’t make you feel good.
"Benefits” of fish oil may be in the form of their ability to suppress the immune system. Unlike seed oils, polyunsaturated fats are so unstable their breakdown products interfere with the production of prostaglandins:
“…fish oils are generally much more immunosuppressive than the seed oils, and the early effects of fish oil on the "immune system" include the suppression of prostaglandin synthesis, because the more highly unsaturated long chain fats interfere with the conversion of linoleic acid into arachidonic acid and prostaglandins. The prostaglandins are so problematic that their suppression is helpful, whether the inhibition is caused by aspirin or vitamin E, or by fish oil.”
Peat explains that the "benefits" of fish oils are similar to the use of X-rays to treat arthritis and ringworm:
“Besides comparing the fish oils to the stronger toxins, another trick is to take advantage of the same immunosuppressive property that had seemed troublesome, and to emphasize their ability to temporarily alleviate some autoimmune or allergic diseases. X-rays were once used that way, to treat arthritis and ringworm, for example.”
The Essentiality of Essential Inflammation
Where were we? Oh yeah, prostaglandins.
Peat is saying they’re all bad and Enig is saying too much is bad, but they’re essential for inflammatory processes needed by the body to repair itself.
In an increased effort to understand Peat's orientation, consider the fact that he rejects the notion of inflammation being a protective mechanism:
"Over the last few decades the meaning of inflammation has changed a little, from being thought of simpley as an essential part of the immune reaction, to being recognized as something that can interfere with the immune system, and that contributes to chronic disease and degeneration."
In an interview with KMUD, Peat explains that the gold standard of "healing" is demonstrated by the fetus, which heals without inflammation in the womb. Peat noted that the large volume of carbon dioxide as well as the placenta acting as a filter for polyunsaturated fat were the mechanisms allowing for this scar-less, inflammation-free, healing.
Fitting in with Ray’s idea with oxidative energy, the largest factor in inflammation may be the ability of cells to produce energy.
A reduction in the metabolic rate causes the release of free fatty acids, shifting cellular metabolism away from mitochondrial use of oxygen to inefficient glycolysis, which increases the production of lactic acid:
"Lactic acid activates the other major mediators of inflammation, including prostaglandins (made from PUFA), free fatty acids (including arachidonate, that forms prostaglandins; Schoonderwoerd, et al., 1989), nitric oxide, carbon monoxide, proteolytic enzymes that degrade the extracellular matrix, TNF (Jensen, et al., 1990), hypoxia inducible factor (Lu, et al., 2002;McFate, et al., 2008), interferon, and interleukins. Arachidonic acid itself can increase lactate production (Meroni, et al., 2003). TNFalpha and interferon gamma activate lactic acid production by increasing prostaglandins (Taylor, et al., 1992)."
Moreover, unsaturated fats influence the production of serotonin:
"An excess of tryptophan in the diet, especially with deficiencies of other nutrients, can combine with inflammation to increase serotonin. Polyunsaturated fatty acids promote the absorption of tryptophan by the brain, and its conversion to serotonin. (A "deficiency" of polyunsaturated fat decreases the expression of the enzyme that synthesizes serotonin [McNamara, et al., 2009)."
Experiment
Limiting unsaturated fatty acids is ideal, but not always possible when one is extremely malnourished. Peat has always maintained that it is the ratio of saturated to unsaturated fat that is the most important factor in getting things back on track. Down the road, it's probably helpful to be more rigorous about the total number of PUFA consumed day in and day out (under a teaspoon per day).
If an abundance of unsaturated fats in the tissue is already present, the use of thyroid, sugar, aspirin, and niacinamide may be warranted.
References:
- Fats, functions & malfunctions by Ray Peat, PhD
- Fats & degeneration by Ray Peat, PhD
- Tripping Lightly Down the Prostaglandin Pathways by Mary Enig, PhD & Sally Fallon
- Precious Yet Perilous by Chris Masterjohn, PhD Candidate
- Aspirin, brain, and cancer by Ray Peat, PhD
- Prostaglandin d2 inhibits hair growth and is elevated in bald scalp of men with androgenetic alopecia.
