In an effort to slash heart disease, the Dietary Guidelines for Americans  have since 1977 been urging people to:
1. Reduce total fat consumption to 30% of total caloric intake.
2. Reduce saturated fat consumption to 10% of total energy intake.
Government issued dietary guidelines are highly authoritative and regarded by a majority as being backed by solid research. However, as it turns out, this is not the case…
Dietary recommendations regarding intake of total and saturated fat are highly controversial, and the debate is heating up. A recent systematic review and meta-analysis of six studies that were available 1977, when the first version of the Dietary Guidelines for Americans was published, shows: 
Population studies show that men with low or low-normal testosterone levels are at an increased risk of mortality compared to those with higher levels, and that cardiovascular disease accounts for the greater proportion of deaths in men with low testosterone.
Here I summarize a medical review paper which addressed the following two questions: 
1. Is testosterone deficiency directly involved in the pathogenesis of these conditions or is it merely a biomarker of ill health and the severity of underlying disease processes?
2. Does testosterone replacement therapy retard disease progression and ultimately enhance the clinical prognosis and survival?
A key hallmark of aging is a progressive loss of muscle mass, which occurs independently of health status. Exercise and nutrition are the two main anabolic stimuli for muscle growth and its maintenance throughout the life course.[2-11]
It is clear that maintaining high physical activity and exercise levels throughout ones lifespan reduces aging related loss of muscle mass and function, compared with living a sedentary life.[12-19]
However, even active older adults and master elite athletes still experience some loss of muscle and physical performance with advancing age.[8, 13, 20]
When it comes to nutrition, high protein intake [2, 3, 10, 21] and creatine supplementation [4-8, 22] are two of the best documented interventions, which together with resistance exercise training, result in greater increases muscle mass and strength in both young [21-23] and older people [2-8, 10], and prevent its loss with aging. Here I will present the relatively unknown effevts of fish oil (most well-known for its cardiovascular health promoting effects) on muscle growth (anabolism) and its possible contribution to prevention of aging related loss of muscle mass and function...
The cardiovascular effects of testosterone and testosterone therapy are subject to intense investigation in medical research and have recently generated heated discussions among healthcare professionals.
While the main focus has been on testosterone per se, it is important to remember that testosterone is both a hormone in its own right, and a pro-hormone that gets converted to both estradiol and DHT (dihydrotestosterone). Estradiol and DHT exert effects themselves that are different from the effects of testosterone.
Therefore, when analyzing the effects of testosterone, especially supplemental testosterone administered as testosterone replacement therapy, it is critical to take into consideration how it affects downstream testosterone metabolites like estradiol and DHT.
Here I will present results from a recent systematic review and meta-analysis that specifically investigated how different routes of testosterone therapy administration (i.e different testosterone preparations) affect blood levels of testosterone and espcially DHT , and how this in turn relates to cardiovascular adverse events.
It is well documented that obesity may cause hypogonadism, and that hypogonadism may cause obesity [1-4] This has generated debate about what condition comes first; obesity or hypogonadism? And what should be the first point of intervention?
In this article I will summarize data from several reviews on the associations of hypogonadism and obesity [1-4], and make the case that these conditions create a self-perpetuating vicious circle. Once a vicious circle has been established, it doesn’t matter where one intervenes; one can either treat the obese condition or treat hypogonadism first. The critical issue is to break the vicious circle as soon as possible before irreversible health damage arises.
Nevertheless, as I will explain here, treating hypogonadism first with testosterone replacement therapy may prove to be a more effective strategy because it to a large extent “automatically” takes care of the excess body fat and metabolic derangements. In addition, treating hypogonadism first also confers psychological benefits that will help obese men become and stay more physically active.
In a previous article "Combined Testosterone and GH therapy for best results on body composition and safety profiles" I covered a study showing that testosterone replacement therapy alone produced significant gains in total lean body mass, leg/arm muscle mass, strength and aerobic endurance, together with significant reductions in whole-body and trunk fat. 
In the same study, addition of GH (growth hormone) further enhanced these beneficial results.
In a follow-up to that that study, the researchers looked deeper into the data with the following analyses: 
- Pathway analysis to test the hypothesis that testosterone and GH affected muscle mass directly and that a threshold change in lean tissue (muscle) mass was needed to generate significant improvements in muscle performance and physical function.
- Bootstrap analysis to determine threshold hormone levels associated with threshold changes in whole-body and appendicular lean mass that would be necessary for improving muscle performance and functional outcomes.
Here I report on the results of this insighful analysis...
Testosterone deficiency is especially common in men who are obese and/or have the metabolic syndrome or diabetes, with a prevalence ranging from 35% to almost 80%.[1-5] However, there is a subgroup of non-obese men who have low testosterone levels and suffer from typical symptoms of low-T, but who do not (yet) have any co-morbidities.
Many studies show that suboptimal testosterone levels may contribute to the development of obesity (including abdominal obesity) [6, 7], metabolic syndrome [8-13] and/or diabetes.[9, 14-20] Therefore, testosterone therapy in non-obese men with testosterone deficiency may be an effective intervention to correct not only symptoms associated with hypogonadism, but also prevent the development of obesity, metabolic syndrome and/or diabetes.
A notable study was set out to specifically investigate this…
A rapidly growing body of medical research is showing that testosterone deficiency (aka hypogonadism and low-T) is strongly associated with a wide range of detrimental health outcomes [1, 2], and that testosterone replacement therapy improves those health parameters that are negatively affected by testosterone deficiency.[2, 3]
Therefore, leading testosterone scientists now view testosterone deficiency as a cardiovascular risk factor that contributes to the development of cardiovascular disease.[4-7]
As general practitioners and cardiologists primarily care for these patients with cardiovascular disease, a survey study was conducted to assess their knowledge, beliefs and clinical practice with respect to testosterone deficiency and cardiovascular health.
During testosterone therapy, total and free estradiol (the main form of estrogen) levels increase dose-dependently in both young (aged 19-35 year old) and 52 older (aged 59-75 year old) men, and more so in older men compared to younger men.
The potential clinical consequences of higher estradiol levels and higher estradiol-to-testosterone ratios in older men remains poorly understood, and the optimal management of high-normal or elevated estrogens is controversial among clinicians.
Interestingly, in some patients, an initial elevation in estradiol is followed by decreased estradiol after prolonged testosterone therapy.[3, 4] This may be due to reduced body fat mass or decreased testosterone levels over time with fixed dose treatments.
Here you will get advice on how to best approach estrogen management while on testosterone therapy…
In a previous article "DHEA – why it is especially important for menopausal women" I explained why DHEA is especially important for women than men, and even more so for peri- and postmenopausal women. In this article, I will cover specific health benefits of DHEA supplementation for menopausal women.
There are indications that women with lower DHEA levels are at higher risk for cardiovascular disease and mortality.[1, 2] In postmenopausal women, lower DHEA(S) levels are linked to higher cardiovascular mortality and all-cause mortality  and lower DHEA(S) levels are also associated with a 41% greater risk of stroke, regardless of other risk factors. These observations are supported by experiments showing that treatment with DHEA reduces experimental atherosclerosis [5-7], improves blood vessel (endothelial) function [8-11], and has anti-inflammatory [12-15] and anti-oxidative effects.[8, 12, 16, 17] Notably, some of the anti-atherosclerotic effects of DHEA are mediated by DHEA on its own, and not via its conversion to estrogen.
Because DHEA is the major source of estrogen and testosterone in post-menopausal women, this begs the question if not all post-menopausal women should supplement with DHEA? Several studies show that DHEA supplementation confers significant health benefits beyond mere relief of menopausal symptoms. Notable are its beneficial effects on the bone, vagina, skin and prevention of breast cancer.