The way it’s reported, you’d think that susceptibility to COVID-19 severity is equally distributed across the world’s population. But when you compare case and mortality rates between countries, differences emerge. There are even differences within countries and states and cities. It’s clear that other variables besides simple exposure to the virus and infection are at play. Research continues to emerge regarding risk factors for severe COVID-19.
What are they?
And, more importantly, can you modify any of the variables?
Male menopause is a real thing, and the medical term for it is andropause. According to the Mayo Clinic, the term “Male Menopause” has been used to describe decreasing testosterone levels related to aging. See this article from Mark back in 2018.
One of the symptoms of male menopause can be erectile dysfunction (ED). Although for younger men, you can have ED without male menopause. ED can destroy a man’s confidence not just in the bedroom but in the larger picture of his life by causing depression, stress, moodiness and anger all things that peak performers do not want to associate with. But for men aged 35-64 these things can sneak up on us, fast.
We are all so busy “performing.” Being a Dad, a good husband, business owner, a hard worker, friend, trying to get your workouts squeezed into an already hectic week. In many cases, this usually leads to a pattern of not not getting enough sleep because of late night emails for work after having put the kids to bed, up early the next day to get right back at your hard charging life, with too little exercise and not enough Primal Nutrition. Which leaves you with high stress. Stress leads to high cortisol (more about cortisol below).
Maybe you had a little too much wine at dinner … it happens. Your wife or lover wants to “play” and so do you, but no response. Once, certainly is nothing to worry about but the definition of ED is “is the recurrent or persistent inability to attain and/or maintain an erection in order for satisfactory sexual performance.” So, what to do?
First, let’s look closer at the leading causes.
Antioxidants serve as a powerful first line of defense against damage to your cells from aging, stress, and inflammation. Moreover, antioxidants appear to contain cancer-fighting properties and to support the immune system (among many other benefits).
Many, many foods, especially colorful vegetables, contain a range of valuable antioxidants. We’ve listed a few of the most potent and popular choices for each class of antioxidants. Here, we’ll go through the most important ones.
When most people worry about getting old, they focus on the obvious degenerative diseases like diabetes and cancer and Alzheimer’s or the catastrophic health emergencies that can occur, like strokes or heart attacks. They think about the melange of medicines they might have to take, the panicked rush to the ER in the dead of night, the slow but unmistakable descent into painful oblivion. But one of the deadliest health conditions afflicting older adults is also one of the most silent and unknown: sarcopenia, or the degeneration and loss of muscle mass and strength. People just don’t think about losing muscle mass and strength as they get older. If they do, they assume it’s just part of the aging process. They figure it’s unavoidable, because, after all, everyone around them just gets weaker and more decrepit as they age. It’s one of those “inevitabilities” that you “just have to accept.” Screw that. Muscle loss is not your destiny. You don’t have to sit there and take it. In fact, sitting there and taking it is the single best way to get sarcopenia; standing up and fighting is the single best way to avoid it. Plus, taking the necessary steps to mitigate or even prevent sarcopenia will help prevent all those other age-related maladies I mentioned in the opening paragraph. Instantly download your Quick Start Guide to a Healthy Gut Health Problems Related to Muscle Atrophy, or Muscle Loss Sarcopenia the specific condition is linked to a number of poor health outcomes: 3.5x higher risk of mortality 3x higher risk of functional decline Greater risk of falls Higher chance of hospitalization Muscle itself is a powerful endocrine organ, emitting hormonal messages that regulate metabolism, inflammation, and overall function. Muscle also provides a metabolic reservoir for support and recovery from physical trauma—injuries, wounds, damage to our tissues. When muscle mass drops to extremely low levels, it means you’re not only more likely to be hospitalized, you’re more likely to never make it out of that hospital bed. Worse still, sarcopenia isn’t just loss of muscle: It’s degradation of the muscle tissue. It’s conversion from fast-twitch Type 2 muscle fibers that can handle heavy loads and high intensity to slow-twitch Type 1 muscle fibers that can only handle lighter loads and lower intensities. It’s the loss of motor units at the muscle itself, forcing the few remaining motor units to pick up the slack and extending recovery times. It’s the loss of cardiac strength, which impairs cardiovascular function and lowers VO2max. It’s the impairment of tendon function, reducing strength and mobility and increasing the risk of injury. Sarcopenia Definition The European Working Group diagnoses sarcopenia if you have two of three conditions: Low muscle mass Low muscle strength Poor physical performance (walking speed, for example) Even if you don’t have full-blown sarcopenia, you may have “pre-sarcopenia.” Millions of people are walking around (or, rather, shuffling around) with lower-than-ideal muscle mass and strength. Today’s post applies to them, too. So whether you’re looking at the … Continue reading “What Is Sarcopenia and How Can You Defeat It?”
Today we’re taking a peek under the hood and looking at some of the hormones involved in hunger and satiety, a.k.a. appetite hormones.
You might think of hunger as a gnawing feeling in your stomach and satiety as that feeling of fullness when you’ve eaten enough… or maybe too much. That’s how we experience the feelings we call hunger and satiety, true; but I’m talking today about the physiological drives to eat or stop eating that is driven by hormones.
Eating behavior is coordinated mostly in the brain by the hypothalamus, which acts as the control center for appetite. Hunger and satiety hormones deliver information from the body about how much energy you are taking in and whether you need more. The overarching goal here is energy homeostasis—balancing the energy coming in (via food) with the energy needed for the everyday functions of being alive.
When you have sufficient energy, your body is free to invest in growth, repair, and reproduction. Taking in more energy than you need can lead to excess fat storage and issues like hyperinsulinemia, insulin resistance, and metabolic syndrome. Energy deficits result in adaptations designed to conserve energy. In the long run, energy deficits might increase longevity, but they can also seriously undermine health and, for example, impair fertility.
Today I’m going to cover some of the key hormones that are involved in this delicate dance. This is by no means a complete list. Let me know in the comments if you have a burning desire to learn more about one of the hormones not covered here.
You can’t change your genes. But you can program them.
The modern world presents a number of problems for our genes. The world we’ve constructed over the last 50 years is not the environment in which our genetic code evolved. Our genes don’t “expect” historically low magnesium levels in soil, spending all day indoors and all night staring into bright blue lights, earning your keep by sitting on your ass, getting your food delivered to your door, communicating with people primarily through strange scratchings that travel through the air. So when these novel environmental stimuli interact with our genetic code, we get disease and dysfunction.
The genes look bad viewed through a modern prism. They get “associated” with certain devastating health conditions. But really, if you were to restore the dietary, behavioral, and ambient environments under which those genes evolved, those genes wouldn’t look so bad anymore. They might even look great.
This is epigenetics: altering the programming language of your genes without altering the genes themselves.