the-psoriasis-treatment

Body fat is not an inert deposit of energy. It can be seen as a distributed endocrine organ. Body fat cells, or adipocytes, secrete a number of different hormones into the bloodstream. Major hormones secreted by adipose tissue are adiponectin and leptin. Estrogen is also secreted by body fat, which is one of the reasons why obesity is associated with infertility. (Yes, abnormally high levels of estrogen can reduce fertility in both men and women.) Moreover, body fat secretes tumor necrosis factor-alpha, a hormone that is associated with generalized inflammation and a number of diseases, including cancer, when in excess. The reduction in circulating tumor necrosis factor-alpha and other pro-inflammatory hormones as one loses weight is one reason why non-obese people usually experience fewer illness symptoms than those who are obese in any given year, other things being equal. For example, the non-obese will have fewer illness episodes that require full rest during the flu season. In tho

With estimates that one out of two white women in North America will suffer from an osteoporotic fracture sometime in their life, prevention of osteoporosis should be a major health objective for all women (and men). In addition, especially in post-menopausal women it is useful to predict the rate of bone loss and to further monitor how bone therapies are assisting over time. Biochemical markers for bone turnover have improved over the last few years (1) and may help with prediction of rate of bone loss. Serum bone alkaline phosphatase, total osteocalcin and procollagen type 1 N-terminal propetide assays are best markers for bone formation (1). N- and C-terminal crosslinked telopeptides in urine and C-terminal telopeptides in serum are sensitive for bone resorption (1). Deoxypiridinoline in urine is another measurement of bone resorption, primarily useful during treatment (2). Monitoring these biochemical markers can be useful for predicting rate of bone loss thereby can be supportive

HDL cholesterol levels are a rough measure of HDL particle quantity in the blood. They actually tell us next to nothing about HDL particle type, although HDL cholesterol increases are usually associated with increases in LDL particle size. This a good thing, since small-dense LDL particles are associated with increased cardiovascular disease. Most blood lipid panels reviewed by family doctors with patients give information about HDL status through measures of HDL cholesterol, provided in one of the standard units (e.g., mg/dl). Study after study shows that HDL cholesterol levels, although imprecise, are a much better predictor of cardiovascular disease than LDL or total cholesterol levels. How high should be one’s HDL cholesterol? The answer to this question is somewhat dependent on each individual’s health profile, but most data suggest that a level greater than 60  mg/dl (1.55 mmol/l) is close to optimal for most people . The figure below (from Eckardstein, 2008; full reference at th

High-density lipoprotein (HDL) is one of the five main types of lipoproteins found in circulation, together with very low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), low-density lipoprotein (LDL), and chylomicrons. After a fatty meal, the blood is filled with chylomicrons, which carry triglycerides (TGAs). The TGAs are transferred to cells from chylomicrons via the activity of enzymes, in the form of free fatty acids (FFAs), which are used by those cells as sources of energy. After delivering FFAs to the cells, the chylomicrons progressively lose their TGA content and “shrink”, eventually being absorbed and recycled by the liver. The liver exports part of the TGAs that it gets from chylomicrons back to cells for use as energy as well, now in the form of VLDL. As VLDL particles deliver TGAs to the cells they shrink in size, similarly to chylomicrons. As they shrink, VLDL particles first become IDL and then LDL particles. The figure below (click on it to enlarge),

An interesting study by Clifton and colleagues (1998; full reference and link at the end of this post) looked at whether LDL cholesterol particle size distribution at baseline (i.e., beginning of the study) for various people was a determinant of lipid profile changes in each of two diets – one low and the other high in fat. This study highlights a few interesting points made in a previous post , which are largely unrelated to the main goal or findings of the study, but that are supported by side findings: - As one increases dietary cholesterol and fat consumption, particularly saturated fat, circulating HDL cholesterol increases significantly. This happens whether one is taking niacin or not, although niacin seems to help, possibly as an independent (not moderating) factor. Increasing serum vitamin D levels, which can be done through sunlight exposure and supplementation, are also known to increase circulating HDL cholesterol. - As one increases dietary cholesterol and fat consumption

Early hominid ancestors like the Australopithecines (e.g., Lucy ) were likely strict vegetarians. Meat consumption seems to have occurred at least occasionally among Homo habilis, with more widespread consumption among Homo erectus, and Homo sapiens (i.e., us). The figure below (from: becominghuman.org; click on it to enlarge) shows a depiction of the human lineage, according to a widely accepted theory developed by Ian Tattersall. As you can see, Neanderthals are on a different branch, and are not believed to have been part of the human lineage. Does the clear move toward increased meat consumption mean that a meat-only diet is optimal for you? The answer is “perhaps”; especially if your ancestors were Inuit and you retained their genetic adaptations. Food specialization tends to increase the chances of extinction of a species, because changes in the environment may lead to the elimination of a single food source, or a limited set of food sources. On a scale from highly specialized to

Ferritin is the body's major iron-storage protein and its levels in serum are parallel to iron stores. Normally, 1 ng/mL of serum ferritin is related to about 8 mg  of iron in storage. It rises somewhat in males and post-menopausal females. Any rise or decrease in levels of serum ferritin indicates available iron stores in the body.  As a diagnostic tool, serum ferritin is the most sensitive test of iron-deficiency anemia in a patient. In presence of iron deficiency, ferritin is generally the first sign followed by decreased iron levels and changes noted in red blood cells such as size, color and number. Low levels of ferritin indicate reduced iron stores or, rarely, malnutrition due to protein depletion. A decrease can also result from hemodialysis. Levels below 10 mg/100 mL is a diagnosis of iron-deficiency anemia.  Higher levels, in contrast, indicate hemochromatosis, hemosiderosis, iron poisoning, or a recent blood transfusion. A higher level of ferritin can also be found in pa

Calcidiol is a pre-hormone that is produced based on vitamin D3 in the liver. Blood concentration of calcidiol is considered to be a reliable indicator of vitamin D status. In the research literature, calcidiol is usually referred to as 25-Hydroxyvitamin or 25(OH)D. Calcidiol is converted in the kidneys into calcitriol, which is the active form of vitamin D. The table below (from: Vieth, 1999; full reference at the end of this post; click on it to enlarge), shows the average blood vitamin D levels of people living or working in sun-rich environments. To convert from nmol/L to ng/mL, divide by 2.496. For example, 100 nmol/L = 100 / 2.496 ng/mL = 40.1 ng/mL. At the time of this writing, Vieth (1999) had 692 citations on Google Scholar, and probably more than that on Web of Science. This article has had, and continues having, a high impact among researchers. The maximum average level of blood (or serum) vitamin D shown in the table is 163 nmol/L (65 ng/mL). Given that the human body produ

Since my recent post on problems related to vitamin D deficiency and excess I received several questions. I have also participated in several discussions in other blogs related to vitamin D in the past few days. There is a lot of consensus about vitamin D deficiency being a problem, but not much about vitamin D in excess being a problem as well. Some bloggers recommend a lot of supplementation, which may be dangerous because: (a) our body evolved to obtain most of its vitamin D from a combination of sunlight exposure and cholesterol, and thus body accumulation regulation mechanisms are not designed to deal with excessive oral supplementation; and (b) vitamin D, like many fat-soluble vitamins, accumulates in fat tissue over time, and is not easily eliminated by the body when in excess. The Vitamin D Council has the following general recommendation regarding supplementation: Take an average of 5,000 IU a day, year-round, if you have some sun exposure. If you have little, or no, sun exp