Blood tests measuring serum levels of total cholesterol with or without lipid profile, pregnenolone, dehydroepiandrosterone sulfate (DHES), progesterone, estrogens and total testosterone levels were done. The follow-up period ranged from 2 to 68 months.
All patients responded to HT (Fig.2). Mean serum total cholesterol dropped by 25.6%-from 254.6 mg/dL before to 188.8 mg/dL after treatment (Fig.3). Serum HDL level (nl >35 mg/dL) decreased from 59.7 mg/dL to 48.0 mg/dL, (19.6% drop), but remained much higher than undesirable levels in all cases (Fig.4).
We believe that a decreasing level of HDL is a very good sign of correct therapy. If we normalize the level of total cholesterol, what reason exists for the extra production of HDL? If there is nothing to transport back to the liver, why produce the extra carrier? HDL, by this logic, should decrease, but in most cholesterol studies (except ours) an HDL increase is reported. Why should the elevation of HDL be a good sign during cholesterol-lowering therapy?
(Editor's note: While the authors make a rational point to explain the decline in HDL using their program, there are numerous studies showing it desirable to maintain the highest possible level of HDL. Those seeking ultimate protection against cardiovascular disease should take steps to maintain high HDL such as moderate intake of niacin, aerobic exercise, consumption of monounsaturated fats (olive and canola oils), reducing excess body fat, avoiding cigarette smoking and even moderate alcohol consumption).
Serum LDL decreased by 23.9% -from 158.2 mg/dL before to 120.4 mg/dL after treatment (Fig.5). During the follow up period no complications or side effects related to HT were a cause for concern. All patients described a significant improvement of quality of life.
In our study we use the term HT (hormonorestorative) with anthropo-identical hormones for treatment of hypercholesterolemia as a name for our regimen. We use this term because there is a lot of confusion with terminology. This term more clearly defines what we are doing during therapy than "HRT." HRT was compromised because it was mainly used in the context of estrogen or estrogen/progestin replacement therapy. Problems with HRT: the majority of studies were performed with only one or two agents, no physiological cyclicity, "one-size-fits-all" (standard dose), no anthropo-identical restoration was attempted, serum hormonal levels were not used clinically and there was a mostly oral route of administration.
The term "natural" HRT is not clear because it is unknown if it is natural for humans or natural for nature, because natural means not human-made, and it may refer to phytoestrogens or equine estrogens. The term "bio-identical to the human hormones" is unambiguous. However, "bio-identical hormones" by itself is confusing ("bios" in Greek is life). In other words, we used hormones that are identical to what humans make and utilize as opposed to what are used in other natural arenas (such as in the bodies of horses). We use the term "anthropo-identical restoration" because it is a more restrictive term than bio-identical ("anthropos" in Greek is human). HT with anthropo-identical hormones means that the chemical structure of the hormones employed is identical to human hormones and the normal ratios between hormones inside of each hormonal group are maintained.
Now we will try to explain some problems from the point of view of our hypothesis. You have heard that if you keep your cholesterol under 200 mg/dl you will be safe against CHD. Right? This is the "conventional wisdom." But it is not necessarily so. We have to remember that a significant proportion of individuals with ischemic heart disease have desirable cholesterol concentration. We know that hypercholesterolemia was observed in 40% to 70% of patients with CAD.53,54 How can we explain that up to 60% of patients with MI have documentated "normal" level of cholesterol?
We will now observe the change of cholesterol in two patients. As you can see, life cycle related elevation of total cholesterol is 60 mg/dl in both cases. We hypothesize that total cholesterol elevation over time is a critical determinant of risk for CHD or MI, not just an absolute number. In our opinion, the risk of heart attack in both cases was equal despite a normal level of cholesterol in the first case.
If we are right and our hypothesis is correct, the normal level of cholesterol during HT must decrease. We made an analysis with five patients with normocholesterolemia (so-called "relative hypercholesterolemia") and the results are given.
It looks like our hypothesis is substantial.
Now we can try to explain why patients with a high level of total cholesterol often have a low level of HDL. In our opinion there exists a so-called "Total cholesterol/HDL paradox." When a patient has a high level of cholesterol that can damage arteries, the body must produce more HDL for the clearing of arteries, but in fact it decreases (a paradox). In this case another mechanism is probably working. It appears that there is no need for an increased production of HDL because there is no excess of cholesterol that must be returned to the liver, barring the fact that there is a high concentration of total cholesterol in the blood. This happens in the case where the body needs more raw materials for the production of hormones, reconstruction of cell membranes (because of a higher risk of aging damage), etc. This sequence represents the working of a self maintaining system.
The following case study presents a typical case of a patient with hypercholesterolemia during HT. This case highlights valuable information about the importance of the relationship between cholesterol and steroidal hormones.