Frequent consumption of red meant and processed meats has been shown in population studies to be associated with cardiovascular disease, cancer and type 2 diabetes [1-3]. It has also been suggested that eating meat increases all-cause mortality . Hence, a high meat intake (regardless of its fat quantity and quality) is generally perceived to be unhealthy and something that should be avoided.
However, although there are many studies documenting these associations, results are not always consistent and there are many important methodological issues which weaken the conclusions (more on that in a bit). In the same way as the putative health risks of red meat consumption is investigated, its documented health benefits (which I will cover below) are equally as important and must be given a fair chance in the establishment of dietary recommendations related to red meat consumption.
In this article I will therefore cover both sides of the red meat debate, and after having taken all the available scientific data into consideration, present a more balanced view about the “meat is bad” dogma…
Some of the most popular supplements today are the so called pre-workout nitric oxide (NO) boosters [1, 2]. These contain a panoply of ingredients, but one the main ones is arginine. The rationale goes that L-arginine is a nitric oxide (NO) precursor and NO is a potent vasodilator [3, 4]. Theoretically this would increase blood flow and nutrient/oxygen delivery to exercising muscles and thereby boost performance, as well as recovery.
While it is true that L-arginine supplementation may be beneficial for various clinical populations (see below), studies in healthy adults have not unequivocally supported the marketing hype surrounding arginine supplementation and nitric oxide boosters [1, 5, 6]. Why? Let's take a look under the hood...
In discussions about diagnosis and health consequences of hypogonadism, aka testosterone deficiency, the prime focus is given to testosterone levels and signs/symptoms.[1-3] However, emerging research has identified a less clinically evident gonadal dysfunction called “subclinical” hypogonadism (or “compensated” hypogonadism).[4, 5]
Subclinical hypogonadism is characterized by normal testosterone levels in the presence of elevated LH level. As testosterone levels are not markedly reduced in subclinical hypogonadism, intuitively one may think it does not confer negative health consequences.
However, a recent study by Corona et al., which specifically was conducted to investigate the potential health ramifications of subclinical hypogonadism, shows that it should not be neglected. Surprisingly, subclinical hypogonadism is associated with an almost 10-fold increased risk of cardiovascular mortality, which is comparable to that for overt hypogonadism! 
One of the most debated issues related to testosterone therapy is its effects on cardiovascular risk and clinical events, like for example heart attack.
January 27th, 2015 a comprehensive medical review paper was published, addressing the controversial topic of testosterone therapy and cardiovascular risk. It was written by the Androgen Study Group academicians and published in Mayo Clinic Proceedings.
Here I summarizes key conclusions from this milestone medical review.
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 Therapy Prevents Gain in Intra-Abdominal Fat and Counteracts Loss of Muscle in Non-Obese Aging Men
- How well informed are general practitioners and cardiologists about testosterone deficiency and its consequences?
- Estrogen elevations in response to Testosterone Therapy – to treat or not?
- DHEA supplementation – specific health benefits for menopausal women