Q: I’m thinking about using chrysin to lower my estrogen. Will it help me cut up or put on muscle?
A: In my opinion, chrysin is ineffective and not worth purchasing. If anyone has any published studies showing otherwise, I’d be more than happy to look at them.
Effective estrogen suppression, however, could lead to hormonal changes affecting body composition. A recent study looking at the effect of anastrozole (brand name Arimidex), a potent aromatase inhibitor used in hormone-suppression therapy for females suffering from breast cancer or other estrogen-sensitive tumors, on males aged 15 to 22 years was published in the Journal of Clinical Endocrinology and Metabolism. It’s known that testosterone deficiency is associated with marked catabolic effects on protein and calcium metabolism and body composition in men that are independent of changes in GH or insulin-like growth factor 1 (IGF-1) production. The purpose of the study was to investigate whether estrogens have a major role in whole-body anabolism in young males.
The subjects took one-milligram doses of Arimidex once a day. The researchers measured protein and bone turnover, hormone levels, metabolic rate and muscle strength at the beginning of the study and after 10 weeks. Contrary to the effects of testosterone withdrawal, there were no significant changes in body composition after estrogen suppression. The authors noted no significant changes in rates of protein synthesis or degradation; carbohydrate, lipid or protein oxidation; muscle strength; calcium kinetics or bone-growth factors concentrations. Additionally, serum bone markers (looking at whether bone was breaking down or building up), osteocalcin and bone alkaline phosphatase concentrations and rates of bone calcium deposition and resorption did not change.
The researchers did note significant changes in serum hormone levels. Estradiol (an estrogen) levels decreased 48 percent. Mean and peak GH concentrations didn’t change, but IGF-1 decreased 18 percent. Testosterone increased 58 percent (wow!) with no change in sex hormone-binding globulin (the protein that binds testosterone, functionally inactivating it). FSH and LH levels both increased significantly. LH is the hormone from the pituitary that signals testosterone production.
The conclusions of the study were that in the male 1) estrogens do not contribute significantly to changes in body composition and protein synthesis; 2) estrogen is a main regulator of the gonadal-pituitary feedback for the gonadotropin axis; and 3) aromatase inhibition, at the level studied, doesn’t negatively affect bone calcium metabolism.
So what does it mean? Well, as a treatment for adolescent boys of short stature, Arimidex may be a means of increasing the height potential by decreasing estrogen levels, since estrogen stops linear bone growth. For bodybuilders and athletes, the hormone changes noted were certainly intriguing. A 58 percent increase in testosterone levels could lead to a positive anabolic environment, although that was not seen in the study. Before clinicians or scientists consider that application, we need to know more about the effect of Arimidex therapy on blood lipids (triglycerides and cholesterol) as well as coagulants and pro-thrombotic factors.
Now, before you get excited and run to the doctor’s office screaming, ‘Arimidex!’ don’t even consider it. Arimidex is an aromatase inhibitor that requires a prescription for approved uses only, such as treating breast cancer. I don’t suggest or condone misuse of pharmaceutical drugs. The only purpose of discussing the study is to suggest possible avenues of future research. There are many conditions in which hyperestrinism (high estrogen levels) affects males or in which wasting conditions may be effectively treated by regimens supporting an anabolic hormonal environment.
Q: Does HCA have any value?
A: HCA is the abbreviation for (-)-hydroxycitrate. It’s been shown in the test tube to act as a competitive inhibitor of the enzyme ATP-citrate lyase. That means it gets in the way of the usual enzyme processes in the cell, leading to greater fatty acid oxidation, or burning. It’s been proposed that HCA interferes with lipogenesis, which is the formation of fat from other sources, like carbohydrates.
There have been conflicting studies regarding the effectiveness of HCA. The argument against the use of Garcinia cambogia, the botanical source for HCA, was clinched in 1998, when the Journal of the American Medical Association published a study in which 1,500 milligrams of HCA daily failed to produce significant weight loss and fat mass loss beyond that observed with a placebo (Heymsfield, et al. 280:1596-1600). Now, the industry behind HCA didn’t let that article pass without fighting its conclusions. In letters to the editor it was criticized on three points: 1) the effectiveness or lack thereof of a product cannot be determined by one study, 2) the low-calorie diet followed in the study negated the HCA’s effectiveness, and 3) the high-fiber diet bound the HCA in the gut, impairing absorption.
Those arguments are sound, but they raise a question: If HCA is so difficult to use effectively that scientists are unable to administer it correctly, then what good is it to the Average Joe or Jane? I’ve received reports from people who have used HCA, and I used it myself for a period. While it does seem to decrease the appetite in a percentage of people, it did not have a noticeable effect on weight loss or, more important, fat loss. A study published in the American Journal of Clinical Nutrition investigated the effects of HCA on carbohydrate and fat metabolism at rest and during exercise in humans (van Loon, et al. 72:1445-1450; 2000). The authors gave their subjects about 4,000 milligrams of HCA twice before a two-hour cycling session and 4,000 milligrams twice more during the cycling. Blood samples demonstrated an increase in blood HCA levels (no wonder, they were taking more than five times the recommended daily dose).
The researchers noted no significant differences in total fat or carbohydrate oxidation, however. Plasma glucose, glycerol and fatty acid concentrations were not significantly different. They concluded that HCA, even when provided in large quantities, does not increase total fat oxidation in endurance-trained athletes.
Now, a fair criticism of that study could be that the actions of HCA are not acute, meaning that levels need to build over the course of days or weeks and that the activities of the enzymes aren’t immediately affected. The short amount of time between administration of the HCA and the measurements may not have allowed for full absorption. Also, it may be argued that the exercising human is not the proper model to study for the effects of HCA. After all, if you’re burning calories in exercise, it’s not likely that the enzymes for converting carbohydrates to fat are going to be active. I’m not jumping to the defense of HCA, but one needs to keep study design in mind when reviewing the research.
Is there any support for the mechanism of HCA? Well, there may be. An experimental drug called C75, which inhibits fatty acid synthase, an enzyme that’s downstream from the ATP-citrate lyase enzyme HCA may affect, has been shown to dramatically decrease food intake and weight. Fatty acid synthase is involved in lipogenesis, and inhibiting it decreases or prevents the synthesis of fatty acids from carbohydrates and amino acids. The New England Journal of Medicine discusses a report by Loftus et al. on treating mice with C75. Injecting C75 into the abdominal cavity led to a doubling of liver concentrations of malonyl-CoA, a precursor in fatty acid synthesis. Daily injections led to rapid and profound weight loss in a dose-dependent manner, with no obvious toxicity. Food intake was decreased by 90 percent! The treated animals lost 45 percent more weight than untreated animals, suggesting that while C75 inhibits feeding, it does not decrease metabolic rates or energy expenditures.
To investigate the idea that C75 leads to a buildup of malonyl-CoA, the researchers injected the animals with a chemical (TOFA) that prevents the accumulation of malonyl-CoA in animals that were already treated with C75. Administering TOFA restored food intake to about two-thirds of normal, supporting the hypothesis that malonyl-CoA is an indicator of fuel status in the brain.
Why is all of that mumbo-jumbo necessary? Well, C75 is a chemical that likely affects weight loss by increasing malonyl-CoA. HCA (remember the original question?) acts by blocking an enzyme upstream from fatty acid synthase, reducing malonyl-CoA levels. Reducing the malonyl-CoA levels has been shown to restore food intake in C75-treated animals. If you look only at those biochemical aspects, the study by Loftus would suggest that HCA should not be effective due to its effect on malonyl-CoA. While the jury is still out, I wouldn’t recommend HCA at this time.
Editor’s note: Daniel Gwartney, M.D., is a clinical pathologist and a graduate of the University of Nebraska College of Medicine. He’s been bodybuilding for more than 18 years. The material presented in this column is for general-information purposes only and is not to be construed as medical advice or an individual recommendation. Consult with your physician or health care provider before embarking on any fitness, training, diet or supplementation program. The author and IRONMAN assume no liability for the information contained in this column. IM