Statins and Sprints: News Alert

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.

Regular Sprints Boost Metabolism

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.

Statins’ Adverse Effects Documented

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.

Further Reading:

10 Rules of Aging Well

The 7 Habits of Healthy (Thin) People

Oprah Hits 200 Pounds. Again.

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25 thoughts on “Statins and Sprints: News Alert”

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  1. Mark,
    Great post! It’s interesting to me to see how, as many people begin to look to lifestyle to cure their ills, rather than to pharmaceuticals to help them maintain their unhealthy lifestyles, the “needs” for these medicines begin to go away.

    For all of the problems I have with the show “The Biggest Loser,” I think the fact that they are showing their contestants need for prescription medications going away this season is a huge boon.

  2. Hey Mark-

    2 Questions on the sprints (and I enjoy them as much as you do – there is just something about running really hard and fast):

    1. How many times per week should someone do these?

    2. I understand that running sprints may be more primal, but what about sprints in the pool, or on the bike? Do they have the same effect physiologically? Might they be even better for you because of the low impact?

    Thanks in advance…

  3. Yep. Your theory just becomes more relevant everyday. But always remember, unlike Ancel Keys and his cronies, the object is trying to disprove your own theory before making it dogma.

  4. In the past, I’ve done Hill Sprints in the past, and have always found them to be really effective. (I can’t do them now, though, as it’s winter in Vancouver). This study doesn’t surprise me at all.

    Same thing with the Statins. I thought about their being a lot of collateral damage when you attach the SYMPTOMS was bang on. That they actually attack the mitochondria is pretty scary.

    – Dave

  5. Mark I’d be interested in your take on products like Promise Activ SuperShots that supposedly remove cholesterol from your body. I’ve seen their commercials a few times now. Seems like another attempt at treating the symptoms instead of the cause.

    Is it reasonable to be concerned that people who don’t have high cholesterol could be adversely impacted usng a product like this?

  6. Excellent news. Gives me even more confidence in sprints, they are my workout of choice when I am pushed for time but need to get outside. 5-7 sets of hill sprints plus some pushups/jumping squats and I’m done!

  7. Speaking of CoQ10. I know there’s a big market for supplementing CoQ10. Currently the only supplements I take are a daily multi-vitamin, fish oil, vitamin D, and ZMA. But as a hard-training athlete, is there any benefit to CoQ10, or anything else for that matter?

  8. Sprinting on the beach is one of my favorite things. I seem to go super slow because of the sand, but geez is it a good workout.

  9. Hey David at AKW!

    “In the past, I’ve done Hill Sprints in the past, and have always found them to be really effective. (I can’t do them now, though, as it’s winter in Vancouver). This study doesn’t surprise me at all.”

    Do the sprints with snowshoes. Awesome awesome workout. With snowshoes, I run fast in the snow for about 50 steps, and then walk for about 30 and repeat. Works just as well as Mark’s beach sprints, I bet.

  10. Fate, I have supplemented with CoQ10 for 15 years. It’s one of those critical nutrients you tend to deplete with age, stress, activity, etc, but you just don’t get much in food. My Damage Control Master Formula was originally designed to provide high levels of hard-to-get antioxidants and other phytonutrients to hard-training athletes.

  11. Ryan, sprints of all types will work. Swimming isn’t quite as productive as running, cycling or even elliptical sprints for these short intense bursts, but if swimming was all you had, you’d still benefit. Once a week is probably enough for running (mostly because if you do it right, it’s not as easy to be fully recovered “injury-preventionwise” as it is from the others). Someone really fit could probabaly do once every 5 days.

  12. Hey Mark….I stopped taking Lipitor on Jan 15th…I feel good like I did a good thing for my body…been on them too long and felt guilty the whole time…geeez….Liked your article…

  13. Facts Believed To Be Qualities Of All Statin Medications:

    Statins are a class of medications specifically prescribed to lower LDL- one of five lipid parameters of a person’s lipid profile, which is alto the name of the blood test to measure these parameters. They are known as statins, as all of these types of medications end with the letters, statin.
    There are about 6 available statins to choose for lipid management as needed- with three that are combination drugs that have a statin in these combinations, I believe.
    There are other classes of medications for lipid management, such as bile acid sequestrants and nicotinic acid, which is known as niacin. Yet the side effect profile is more unfavorable of these classes of medications compared with the statin class of drugs.
    One’s cholesterol level is primarily due to how they produce cholesterol in their liver, which is overall genetically determined. This level is also determined by one’s lifestyle and diet as well. If a person has too much cholesterol in their blood, it can lead to hardening and narrowing of their arteries as well as the formation of coronary plaques in the coronary arteries.
    If these plaques break off of the arterial wall, this leads to a myocardial infarction, or heart attack. Statins are believed to stabilize coronary plaques so this does not occur.
    To measure one’s cholesterol, a blood test called a lipid profile is obtained from a person after they have fasted for at least 12 hours. The test should also be performed only if the person is free of any acute illness, as this may affect true lipid measures.
    If the results prove to be abnormal, lipid altering medicinal therapy may be initiated- according to the discretion of the person’s health care provider. This therapy usually involves a statin medication.
    Adverse events associated with the statin class of pharmaceuticals are thought to occur more often than they are reported- with high doses of statins prescribed to patients in particular at times that may not be necessary to control their dyslipidemia based on their lipid profile. Side effects may include muscle pain, or possible damage to the patient’s liver.
    However, since this class of statin drugs has existed for use for over 20 years, statins are considered to be overall safe and effective for enhancing the clearance of LDL noted to be elevated in the lipid profiles of patients.
    Also, they have proven to reduce cardiovascular mortality with one who is treated with a statin that has dyslipidemia. In addition to lowering LDL by up to about 60 percent- depending on the choice of the statin prescribed for the patient, and how high the LDL cholesterol is in a patient.
    This class of drugs also has the ability to raise their HDL lipid parameter as well as lower to their benefit their triglyceride parameter of their lipid profile. Both of these additional effects in addition to lowering the LDL parameter from taking a statin drug is ultimately beneficial for the patient on a statin drug for lipid management.
    Statin therapy is also recommended for those patients who have a greater than twenty percent risk of developing cardiovascular disease, or those patients that have clinical evidence of this disease.
    Additionally, there appears to be no comparable reduction in cardiovascular morbidity or mortality, as well as a difference in the increase of one’s lifespan, if one is on any particular statin medication for their lipid management over another, others have concluded. So caution should perhaps be considered if one chooses to prescribe a statin for a patient if they are absent of, or have only mild dyslipidemia to a significant degree.
    Furthermore, research should be done by the health care provider if they are under the belief that one statin medication provides a greater cardiovascular benefit over another. In other words, the health care provider should be assured that any choice of statin therapy for their patients is considered reasonable and necessary if the LDL in their patients need to be reduced, and the statin selection should be determined by the results that have been shown with a particular statin.
    There exist abstract etiologies for health care providers at times to choose to prescribe statin drugs on occasion for reasons not indicated with the medicinal treatment of these statin drugs. Examples include the speculated benefits associated with statins- such as reducing CRP levels, or for Alzheimer’s treatment, or other reasons not directly related to cholesterol management.
    Statin therapy for such patients may not be considered appropriate, reasonable, or necessary prophylaxis at this point for any patient who does not have the indications for which statins are approved for to treat patients with dyslipidemia. All other benefits that appear to have favorable effects in such areas not involved with a patient’s cholesterol are suggested at this point due to minimal research in these other variables aside from lipid management.
    Other reasons for placing a patient on a statin drug at this time require further research for these disease states and dysfunctions that may exist with a patient aside from dyslipidemia.
    Statins as a class of drugs seem to in fact decrease the risk of cardiovascular events significantly, it has been proven. Statins also decrease thrombus formation as well as modulate inflammatory responses (CRP) as additional benefits of the medication.
    For those patients with dyslipidemia who are placed on a statin, the effects of that statin on reducing a patient’s LDL level can be measured after about five weeks of therapy on a particular statin drug.
    Liver Function blood tests are recommended for those patients on continued statin therapy, and most are chronically taking statins for the rest of their lives to manage their lipid profile in regards to maintaining the suitable LDL level for a particular patient presently. Patients should be made aware of potential additional side effects as well, such as myopathy and muscular dysfunctions that occur on occasion when one is on statin therapy.

    Yet some have said that about half of all strokes and heart attacks that do occur are not because of increased cholesterol levels of these patients. So it appears clear that high cholesterol may not be an absolute for cardiovascular events for them to occur.
    Others believe that it is oxidized cholesterol that causes vulnerable plaques to form on coronary arterial walls, which is the catalyst for a heart attack, and that there is no medicinal treatment for the formation or stabilization of these plaques to prevent heart attacks or strokes.
    Some who support statin medicinal therapy for their clinically appropriate patients claim that these drugs, do, in fact, stabilize these plaques as an added benefit, and therefore are beneficial.
    As stated previously, in regards to other uses of statins besides just primarily LDL reduction, there is some evidence to suggest that statins have other benefits besides lowering LDL, but not enough evidence yet.
    These other disease states include aside from what has been stated already, such as those patients with neurological disease, as well as statins being beneficial for certain cancer patients. Some have suggested that statins interfere with cancer treatment with bladder cancer patients as well. Yet again, these other roles for statin therapy have only been minimally explored and researched, comparatively speaking.
    Because of the limited evidence regarding additional benefits of statin medications, the drug should again be prescribed for those with dyslipidemia only at this time involving elevated LDL levels as detected in the patient’s bloodstream.
    Yet overall, the existing cholesterol lowering recommendations or guidelines should possibly be re-evaluated. The cholesterol guidelines that presently exist may be over-exaggerated possibly due to tacit suggestions from the makers of statins to those who create these current lipid lowering guidelines.
    This is notable if one chooses to compare these cholesterol guidelines with the other guidelines that have existed in the past. The cholesterol guidelines that exist now are considered by many health care providers and experts to be rather unreasonable and unnecessary, as well as possibly have the potential to be detrimental to a patient’s health.
    Yet statins are beneficial medications for those many people that exist with elevated LDL levels that can cause cardiovascular events to occur because of this abnormality. What that ideal LDL level is may have yet to be empirically determined.
    Finally, a focus on children and their lifestyles should be amplified so their arteries do not become those of one who is middle-aged, and this may prevent them from being candidates for statin therapy now and in the future, regarding the high cholesterol issue. Treating children with a statin drug for dyslipidemia is controversial presently. Dietary management should be the first consideration in regards to correcting lipid dysfunctions that may exist in patients,
    Dan Abshear

  14. My experience, which is not untypical: simvastatin more or less halved my LDL but did nothing to affect my abysmal HDL and trigs, which I now realise were the result of the Heart Healthy diet and got significantly worse when I was told to further reduce my fat consumption and eat more carbs.

    Switching to a low carb diet slashed my trigs to 10% of their original number and doubled HDL. My LDL increased slightly but my GP wasn’t fussed, as she appears to have read some of the same stuff the rest of us have read.

    She was a bit more fussed when I discovered increasing my sat fats increased HDL and decreased LDL by about the same amount (like me she is of the generation brought up to believe fats are the spawn of the devil) and I’m not going to tell her until after the results that I intend dropping the statin for a month prior to my next bloods to see what my unmedicated lipids come out to.

    Just as dietary fats are only dangerous in the presence of toxic levels of carbs I suspect LDL is only dangerous in the presence of toxic levels of trigs and reduced HDL. My body, my science experiment . . .

    . . . it may be I will need to remain on them, some people have crap lipids whatever they eat or do,but in terms of reducing cardiovascular risk diet has beaten statins hands down in my body.

  15. Statins suck. If everyone slowly but surely changed their lifestyles to be more grok-like, maybe the health care crisis would shrink proportionally with peoples’ waistlines. As an xray tech, maybe I’d be dealing more with the occassional fracture instead of chests and bellies on patients who need to be lifted with cranes.

  16. Agree with dietary and exercise approaches as primary prevention (before an MI) first. Always. Many patients do NOT need statins.

    Nevertheless, many people fail to make appropriate lifestyle changes or have genetically based significantly abnormal LDL levels despite dramatic lifestyle changes. For them, and especially for those with already established blood vessel disease, statins have demonstrated benefits in randomized studies showing patients live longer and have fewer cardiovascular events. Unlike much of medicine, this is unambiguous and unassailable for these specific contexts. A brief lay article:,8599,1878543,00.html

    1. @Doc in Chicago, how come the link you provide is to a Mayo Clnic article on the benefits of statins? I disagree with your assessment. The Time article references a “study” where 30 fewer people out of a study group of 8,901 high risk people had an “event” (meaning a heart attack or stroke) and then went on to claim that it represented a reduction in risk of about 50%. That’s relative risk in a high risk group. I hardly call that unambiguous and/or unassailable.

  17. My question is regarding coQ10.

    I am going to turn 40… am in good health… exercise regularly and have been primal for about 2 years.

    Here are my two questions…

    How much coQ10 do I require?

    What is the deal with all the coQ10 supplements using seed and or soybean oil as the vehicle? I can not find one using say olive oil. Any advice on this? Or does it not matter?

    Your thoughts?


  18. Just got results of my Calcium Heart CT Scan with calcium accumulation in 1 coronary artery and the Dr wants to go down the Statin road..
    Back Ground
    53 yrs old Male
    I have been on daily asprin (325mg) for years and more or less been on a carb restricted diet for a couple of years. About 4 weeks ago started a Very low Carb routine (less than 50gm / day) increasing protein & fat intake. Dropped ALL grains & stopped using beans as my carb source. Yes i do have the Primal Blue Print as well as several other books on Low Carb Eating. Results from recent physical BP was 116/65, HR was 62 bpm,

    TG level was 86, HDL 36 & Calculated LDL 72,

    Fasting Glucose was 98 (always my highest reading) and my A1C reading was 4.8 (down from a 5.0 last year.

    According the research i have been gathering the LDL levels can be fairly inaccurate and that a better marker is to compare the TG/HDL value with 3.5 being the marker between Pattern A(light and bouyant) & B(small & dense) LDL particles and i am at 2.5 wich puts me in the preferred Pattern A LDL…

    With my already LOW HDL & my existing fasting glucose making me predisposed to Type II Diabetes i am noit to thrilled about starting a Statin drug. I plan to continue with my current eating routine at 35% Protein, 60% Fats & 5% Carbs which will likely cause my GP to think i have slipped off the reservation.

    Now for My Question is there anything diet or exercise that will reduce the existing calcium buildup in my coronary arteries?