You’ve probably noticed that we like to revisit subjects, no matter how exhaustive our prior analysis may have appeared. We do this for two reasons – to foster a running dialogue on a constantly evolving idea; and to make sure the Primal Blueprint remains supported by hard science.
Mark has always talked about his affection for the beach sprint (or any type of sprint) as a quick, intense, effective cardio workout in line with the type of daily activities Grok performed. He’s also conveyed his unease with our increasing reliance on Big Pharma for our health and wellness needs. Today’s post deals with two recent studies of particular interest and relevance to these topics. We found them quite interesting, and we think our readers might too.
A team of Scottish researchers, interested in the metabolic effects of high intensity interval training (HIIT), examined a group of sixteen sedentary male patients (abstract and full study – PDF). They plopped them down on stationary bikes and had them do interval sprints for no more than a few minutes at a time. The researchers acknowledged the current mainstream guidelines (low-moderate intensity exercise for several hours per week) as effective, but unrealistic for busy people without much time for exercise. But what started as a simple look at intense interval training as a temporary holdover for the time-strapped soon became a revelation: HIIT appeared to actually be more effective at raising metabolism and “improving insulin action and glucose clearance,” leading researchers to conclude that they “do not yet understand the traditional connection between exercise and diabetes.”
Perhaps more research of this ilk would help, and we’ll be sure to highlight it as it comes out.
You know by now that we don’t care for statins. We find them unnecessary and overly restrictive, and they generate a lot of money for the wrong reasons. Oh, sure, statins lower cholesterol by retarding our bodies’ natural cholesterol-producing mechanisms (while other drugs reduce our ability to absorb dietary cholesterol), but they operate under an inherently flawed assumption: that cholesterol is the devil.
As we’ve discussed before, cholesterol is necessary for proper functioning of the body. Universally-praised HDL transports excess cholesterol to the liver when the body’s through with it; universally-maligned LDL transports cholesterol from the liver to the tissues. All LDL gets the bad rap, but it’s not that simple. The lighter, billowy LDL is quite benign, but the smaller, denser LDL particles are the ones that have been linked to heart disease (unsurprisingly, these tiny LDL particles are caused by a diet high in simple carbs). But as is Big Pharma’s tendency, their solution is to just carpet-bomb the whole lot. Their statins attack the symptoms, but they don’t get to the root of the problem.
As with any instance of overwhelming firepower directed at the symptoms, rather than the true cause, there’s a lot of collateral damage. Statins, we’re finding, wreak considerable collateral damage – muscle problems, cognitive issues, pain and numbness in the extremities, tendon problems, and blood glucose elevations, to name a few.
Now they have it on paper – entombed, published, unavoidable – that statins, those vaunted anti-cholesterol tablets that comprise so many of our parents’ and grandparents’ pill boxes, might be causing more damage than they’re worth (gee, really?). The paper (co-authored by the UCSD Statin Study director) suggests that statin-induced damage to the body’s mitochondria is the true cause of the commonly-reported side effects of statin use.
Mitochondria are pretty damn essential. Thanks to Coenzyme “Q10,” (CoQ10), mitochondria produce energy and fight free radicals. Unfortunately for statin-users, CoQ10 travels along the same pathway as some types of cholesterol. Following its scorched-earth policy to a tee, statins block that pathway, meaning CoQ10 can’t get through to help mitochondria destroy free radicals. More free radicals running rampant means more inflammation – which is the true cause of heart disease.
So, do the study’s authors conclude that statins might actually increase the risk of heart disease? Not quite. In the authors’ own words, statins may “protect against the very same problems, in some people, to which they may predispose others.” It’s muddled language, but it’s pretty clear to us that relying on statins to reduce the risk of heart disease is – to be diplomatic – rather counterproductive.