Kris Kresser: Why has the American approach to heart disease failed?

Why Has the American Approach to Heart Disease Failed?
on April 18, 2017 by Chris Kresser 

Tsimane 2

A recent New York Times article correctly suggests that diet and lifestyle changes are far more effective ways to prevent and treat heart disease than statins and stents. But what diet, and what lifestyle? Is it as simple as avoiding “artery-clogging saturated fat,” as the author suggests? Read on to find out why the American approach to heart disease has really failed.
Jane Brody wrote an article in The New York Times called “Learning from Our Parents’ Heart Health Mistakes.” She argues that despite decades of advice to change our diet and lifestyle in order to reduce our risk of heart disease, we still depend far too much on drugs and expensive procedures like stents.
She says:
Too often, the American approach to heart disease amounts to shutting the barn door after the horse has escaped.
To support this argument, she refers to a recent paper published on the Tsimane, an indigenous population in the Bolivian Amazon. The study found that the rate of coronary atherosclerosis in the Tsimane was one-fifth of that observed in the United States (and the lowest that has ever been measured). Nearly nine in 10 Tsimane had unobstructed coronary arteries and no evidence of heart disease, and the researchers estimated that the average 80-year-old Tsimane has the same vascular age as an American in his mid-50s.
I certainly agree with Ms. Brody so far, and her analogy that the American approach to heart disease amounts to shutting the barn door after the horse has escaped is spot on.
The problem is what comes next, as she attempts to answer the question of why the Tsimane have so much less heart disease than Americans:
Protein accounts for 14 percent of their calories and comes primarily from animal meats that, unlike American meats, are very low in artery-clogging saturated fat. [emphasis mine]
Does saturated fat “clog” your arteries?
Artery-clogging saturated fat? Are we still using that phrase in 2017?
As I’ve written before, on average, long-term studies do not show an association between saturated fat intake and blood cholesterol levels. (1) (I say “on average” because individual response to saturated fat can vary based on genetics and other factors—but this is a subject for another article.)
If you’re wondering whether saturated fat may contribute to heart disease in some way that isn’t related to cholesterol, a large meta-analysis of prospective studies involving close to 350,000 participants found no association between saturated fat and heart disease. (2)

Does saturated fat really “clog” your arteries?

Are “clogged arteries” the cause of heart disease?
Moreover, as Peter Attia eloquently and thoroughly described in this article, the notion that atherosclerosis is caused by “clogged arteries” was shown to be false many years ago:
Most people, doctors included, think atherosclerosis is a luminal-narrowing condition—a so-called “pipe narrowing” condition.  But by the time that happens, eleven other pathologic things have already happened and you’ve missed the opportunity for the most impactful intervention to prevent the cascade of events from occurring at all.
To reiterate: atherosclerosis development begins with plaque accumulation in the vessel wall, which is accompanied by expansion of the outer vessel wall without a change in the size of the lumen. Only in advanced disease, and after significant plaque accumulation, does the lumen narrow.
Michael Rothenberg also published an article on the fallacy of the “clogged pipe” hypothesis of heart disease. He said:
Although the image of coronary arteries as kitchen pipes clogged with fat is simple, familiar, and evocative, it is also wrong.
If heart disease isn’t caused by “clogged arteries,” what does cause it?
The answer to that question is a little more complex. For a condensed version, read my article “The Diet-Heart Myth: Why Everyone Should Know Their LDL Particle Number.”

For a deeper dive, read Dr. Attia’s article.
Here’s the 15-second version, courtesy of Dr. Attia:
Atherosclerosis is caused by an inflammatory response to sterols in artery walls. Sterol delivery is lipoprotein-mediated, and therefore much better predicted by the number of lipoprotein particles (LDL-P) than by the cholesterol they carry (LDL-C).
You might think that I’m splitting hairs here over terminology, but that’s not the case. It turns out that this distinction—viewing heart disease as caused by high LDL-P and inflammation, rather than arteries clogged by saturated fat—has crucial implications when it comes to the discussion of how to prevent it.
Because while it’s true that a high intake of saturated fat can elevate LDL particle number in some people, this appears to be a minority of the population. The most common cause of high LDL-P in Americans—and elsewhere in the industrial world—is almost certainly insulin resistance and metabolic syndrome. (I explain why in this article.)
And what is one of the most effective ways of treating insulin resistance and metabolic syndrome? That’s right: a low-carbohydrate, high-fat diet!
News flash: diets high in saturated fat may actually prevent heart disease.
Perhaps this explains why low-carbohydrate, high-fat diets (yes, including saturated fat) have been shown to reduce the risk of heart disease.
For example, a meta-analysis of 17 low-carb diet trials covering 1,140 obese patients published in the journal Obesity Reviews found that low-carb diets were associated with significant decreases in body weight, as well as improvements in several CV risk factors, including decreases in triglycerides, fasting glucose, blood pressure, body mass index, abdominal circumference, plasma insulin, and C-reactive protein, as well as an increase in HDL cholesterol. (3)
(In case you’re wondering, low-carb diets in these studies had a null effect on LDL cholesterol: they neither increased nor decreased it.)
Saturated fat is a red herring.
Instead of focusing so much on saturated fat intake, which is almost certainly a red herring, why not focus on other aspects of the Tsimane’s diet and lifestyle that might contribute to their low risk of heart disease?

For example:
They are extremely active physically; Tsimane men walk an average of 17,000 steps a day, and Tsimane women walk an average of 15,000 steps a day—and they don’t sit for long periods. Ms. Brody does mention this in her article.
They don’t eat processed and refined foods. We have been far too focused on calories and macronutrient ratios and not enough on food quality. We now know that hunter–gatherers and pastoralists around the world have thrived on both high-carbohydrate, low-fat diets (like the Tsimane, who get 72 percent of calories from carbohydrate) and low-carbohydrate, high-fat diets (like the Masai and Inuit).

But what all hunter–gatherer diets share in common is their complete absence of processed and refined foods.
Perhaps if we stopped focusing so much on the amount of fat and carbohydrate in our diet and started focusing more on the quality of the food we eat, we’d be better off.
And of course we also need to attend to the many other differences between our modern lifestyle (which causes heart disease) and the ancestral lifestyle (which prevents it), including physical activity, sleep, stress, light exposure, play/fun, and social support.
The Tsimane study illustrates exactly why an evolutionary perspective on diet, lifestyle, and behavior is so important. It helps us to generate hypotheses on what aspects of our modern way of life may be contributing to chronic diseases like atherosclerosis and gives us ideas about what interventions we need to make to prevent and reverse these diseases.

Sheri Colberg: Joint health is critical to staying active

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Joint Health Is Critical to Staying Active

Diabetes in Control

Without properly functioning joints, our bodies would be unable to bend, flex, or even move. A joint is wherever two bones come together, held in place by tendons that cross the joint and attach muscles to a bone on the other side and ligaments that attach to bones on both sides of the joint to stabilize it. The ends of the bones are covered with cartilage, a white substance formed by specialized cells called chondrocytes. These cells produce large amounts of an extracellular matrix composed of collagen fibers, proteoglycan, elastin fibers, and water. Tendons and ligaments are also made up primarily of collagen.

Joints can be damaged, however, making movement more difficult or painful. Joint cartilage can be damaged by acute injuries (i.e., ankle sprain, tendon or ligament tears) or overuse (related to repetition of joint movements and wear-and-tear over time). Damage to the thin cartilage layer covering the ends of the bones is not repaired by the body easily or well, mainly because cartilage lacks its own blood supply.

Aging alone can lead to some loss of this articular cartilage layer in knee, hip, and other joints—leading to osteoarthritis and joint pain—but having diabetes also potentially speeds up damage to joint surfaces. Although everyone gets stiffer joints with aging, diabetes accelerates the usual loss of flexibility by changing the structure of collagen in the joints, tendons, and ligaments. In short, glucose “sticking” to joint surfaces and collagen makes people with diabetes more prone to overuse injuries like tendinitis and frozen shoulder (1; 2). It may also take longer for their joint injuries to heal properly, especially if blood glucose levels are not managed effectively. What’s more, having reduced motion around joints increases the likelihood of injuries, falls, and self-imposed physical inactivity due to fear of falling.

Reduced flexibility limits movement around joints, increases the likelihood of orthopedic injuries, and presents a greater risk of joint-related problems often associated with diabetes, such as diabetic frozen shoulder, tendinitis, trigger finger, and carpal tunnel syndrome. These joint issues can come on with no warning and for no apparent reason, even if an individual exercises regularly and moderately, and they may recur more easily as well (3). It is not always just due to diabetes, though, since older adults without diabetes experience inflamed joints more readily than when they were younger.

So what can you do to keep your joints mobile if you’re aging (as we all are) and have diabetes? Regular stretching to keep full motion around joints can help prevent some of these problems, and also include specific resistance exercises that strengthen the muscles surrounding affected joints. Vary activities to stress joints differently each day. Overuse injuries occur following excessive use the same joints and muscle in a similar way over an extended period of weeks or months, or they can result from doing too much too soon.

Doing moderate aerobic activity that is weight-bearing (like walking) will actually improve arthritis pain in hips and knees (4). People can also try non-weight-bearing activities, such as aquatic activities that allow joints to be moved more fluidly. Swimming and aquatic classes (like water aerobics) in either shallow or deep water are both appropriate and challenging activities to improve joint mobility, overall strength, and aerobic fitness. Walking in a pool (with or without a flotation belt around the waist), recumbent stationary cycling, upper-body exercises, seated aerobic workouts, and resistance activities will give you additional options to try.

Finally, managing blood glucose levels effectively is also important to limit changes to collagen structures related to hyperglycemia. Losing excess weight and keeping body weight lower will decrease the risk for excessive stress on joints that can lead to lower body joint osteoarthritis (5). Simply staying as active as possible is also critical to allowing your joints to age well, but remember to rest inflamed joints properly to give them a chance to heal properly. You may have to try some new activities as you age to work around your joint limitations, but a side benefit is that you may find some of them to be enjoyable!

References:

  1. Abate M, Schiavone C, Pelotti P, Salini V: Limited joint mobility in diabetes and ageing: Recent advances in pathogenesis and therapy. Int J Immunopathol Pharmacol 2011;23:997-1003
  2. Ranger TA, Wong AM, Cook JL, Gaida JE: Is there an association between tendinopathy and diabetes mellitus? A systematic review with meta-analysis. Br J Sports Med 2015;
  3. Rozental TD, Zurakowski D, Blazar PE: Trigger finger: Prognostic indicators of recurrence following corticosteroid injection. J Bone Joint Surg Am 2008;90:1665-1672
  4. Rogers LQ, Macera CA, Hootman JM, Ainsworth BE, Blairi SN: The association between joint stress from physical activity and self-reported osteoarthritis: An analysis of the Cooper Clinic data. Osteoarthritis Cartilage 2002;10:617-622
  5. Magrans-Courtney T, Wilborn C, Rasmussen C, Ferreira M, Greenwood L, Campbell B, Kerksick CM, Nassar E, Li R, Iosia M, Cooke M, Dugan K, Willoughby D, Soliah L, Kreider RB: Effects of diet type and supplementation of glucosamine, chondroitin, and msm on body composition, functional status, and markers of health in women with knee osteoarthritis initiating a resistance-based exercise and weight loss program. J Int Soc Sports Nutr 2011;8:8

 

In addition to my educational web site, Diabetes Motion (www.diabetesmotion.com), I also recently founded an academy for fitness and other professionals seeking continuing education enabling them to effectively work with people with diabetes and exercise: Diabetes Motion Academy, accessible at www.dmacademy.com. Please visit those sites and my personal one (www.shericolberg.com) for more useful information about being active with diabetes.

Keep safe when cycling

cyclist

Reflective jackets are a great safety aid for cyclists riding in the dark, if they have them and  wear them consistently. A possible way to overcome a cyclists reluctance to wear the said jacket, say for example if they think to themselves, “I’ll be back before it gets dark or it’s too warm for my jacket” is to take the decision out of the equation.

Researchers have found that reflective tape attached to the rear frame of the bike and pedal cranks does the job of increasing visibility just as well as jackets do, but without any active behaviour required of the cyclist.

“Reflective tape is highly recommended to complement front and back lights in bicycle riding at night”, they conclude.

Human Factors, 2016, doi:10.177/001872081667145

Adapted from article in Human Givens Volume 24 No 1 2017

Limited time to exercise? Weekend warriors still benefit

Marines_do_pushups
From bootcamps to ballet, there’s a work-out for everyone on YouTube.

From BMJ 14th January 2017

Although guidelines recommend spreading exercise throughout the week, weekend warriors, who compress the recommended amount into the weekend, still experience substantial benefits.

JAMA Internal Medicine reported that risk of death from all causes were 30% down, cardiovascular disease deaths were 40% down  and cancer deaths were 18% down, compared to inactive adults. 

(doi:10.1136/bmj.j126)

Weight loss increases hunger: a major obstacle for maintenance

weight-lossWe  know about the issue of slowed metabolism after weight loss due to the lean muscle mass loss that goes along with fat loss. This is one reason why higher protein/low carb diets work better than low fat diets; because muscle mass is maintained better. Well, new information from Diabetes in Control backs up what some of us know intuitively or may have experienced personally….

Losing Weight Increases Hunger

The study showed that for every kg of weight they lost, patients consumed an extra 100 calories a day — more than three times what they would need to maintain the lower weight.

This out-of-proportion increase in appetite when patients lost a small amount of weight may explain why maintaining long-term reduced body weight is so difficult.

A validated mathematical method was used to calculate energy intake changes during a 52-week placebo-controlled trial in 153 patients treated with canagliflozin, a sodium glucose co-transporter inhibitor that increases urinary glucose excretion, thereby resulting in weight loss without patients being directly aware of the energy deficit. The relationship between the body weight time course and the calculated energy intake changes was analyzed using principles from engineering control theory.

Previous studies show that metabolism slows when patients lose weight; however, these results suggest that proportional increases in appetite likely play an even more important role in weight plateaus and weight regain.

Knowing that patients with type 2 diabetes who receive the sodium-glucose cotransporter 2 (SGLT-2) inhibitor canagliflozin (Invokana) as part of a glucose-lowering strategy excrete a fixed amount of glucose in the urine (which causes weight loss), they used a mathematical model to calculate energy-intake changes during a 52-week placebo-controlled trial of the drug, in which 153 patients received 300-mg/day canagliflozin and 89 patients received placebo.  Using this approach meant that the participants who received canagliflozin consistently excreted 90-g/day glucose but were not aware of the energy deficit.

Previously, the researchers had validated a mathematical model to calculate the expected changes in caloric intake corresponding to changes in body weight (Am J Clin Nutr. 2015;102:353-358). They input the current study data into this model.

At study end, the patients who had received placebo had lost less than 1 kg and those who had received canagliflozin had lost about 4 kg. The weight loss with canagliflozin was less than predicted, due to the patients’ increased appetite. On average, patients who received canagliflozin ate about 100 kcal/day more per kg of weight lost — an amount more than threefold larger than the corresponding energy-expenditure adaptations.

“Our results provide the first quantification of the energy-intake feedback-control system in free-living humans,” the researchers write.

They add that in the absence of “ongoing efforts to restrain food intake following weight loss, feedback control of energy intake will result in eating above baseline levels with an accompanying acceleration of weight regain.”

The findings suggest that “a relatively modest increased appetite might explain a lot of the difficulty that people are having in both losing the weight and maintaining that weight loss over time. From the results it was concluded that, while energy expenditure adaptations have often been considered the main reason for slowing of weight loss and subsequent regain, feedback control of energy intake plays an even larger role and helps explain why long-term maintenance of a reduced body weight is so difficult.

The findings suggest that an increased appetite is an even stronger driver of weight regain than slowed metabolism. “The message to clinicians is to not only push physical activity as a way to counter weight regain but also use medications that impact appetite.”

In summary, the researchers conclude the few individuals who successfully maintain weight loss over the long term do so by heroic and vigilant efforts to maintain behavior changes in the face of increased appetite along with persistent suppression of energy expenditure in an omnipresent obesogenic environment. Permanently subverting or countering this feedback control system poses a major challenge for the development of effective obesity therapies.

Practice Pearls:

  • Findings suggest that an increased appetite is an even stronger driver of weight regain than slowed metabolism.
  • Appetite increased by ∼100 kcal/day above baseline per kilogram of lost weight.
  • The message to clinicians is to not only push physical activity as a way to counter weight regain, but also use medications that impact appetite.

Obesity. 2016;24:2289-2295. Abstract

Weight plateaus are a normal, but frustrating, feature of your weight loss journey

frustration

 Here are some words of wisdom and encouragement from a health care professional who knows how discouraging weight loss plateaus can be. Don’t let weight stabilisation lead you to jack in your efforts.
When Losing Weight, Warn ‘em!

Diabetes in Control November 8th 2016

I work in obesity medicine. As many of us know, losing weight isn’t the problem for most, but weight regain is.

As the saying goes for many, you can’t be rich enough or thin enough. Many of our patients come in with unrealistic goals regarding their weight loss, and don’t give themselves enough credit for the weight they have lost. Many, for many reasons, regain.
Woman, 58 years of age, class II obesity, prediabetes (A1C 6.0%), HO depression, on antidepressants, weight of 188, BMI 38. Started on metformin and lower carb meal plan.
Warned her early on it’s not just about losing weight, but what’s important is keeping it off. We need plans for both.
Her treatment plan does not end when she loses weight.  Over 6 months she lost 22 pounds. This is a 12% weight loss. BMI 33.5 now.  No further weight loss since the 6-month period, but no weight gain.
Patient frustrated. She has upped her exercise. No longer wants to continue metformin. Encouraged her to continue her meal plan, metformin and bump up her exercise plan. Praised her for her weight loss and not regaining.  And, reminded her this is what we discussed from the start. She remembered and said she’ll stay with the plan.
Lessons Learned:
  • Keeping weight off is a different stage of the weight loss journey.
  • Reminder that losing 3-5% total body weight can improve health outcomes.
  • 5-7% weight loss was shown in the DPP to prevent or delay type 2 diabetes.
  • From the beginning, let patients know there are stages to losing weight. First is to lose, then it’s to keep off the weight lost. Make a plan for both.
  • Regarding weight loss, put more emphasis on the food side.
  • Regarding weight maintenance, put more emphasis on exercise.
  • Remind patient of discussion and encourage patient to embrace the weight loss they have been able to achieve and keep off.

Anonymous

Most people need a minimum of one hour exercise a day

walking

How Much Exercise Compensates for Sitting at a Desk for eight Hours A Day?

Diabetes in Control August 27th 2016

At least an hour of physical activity needed to offset risk for several chronic conditions and mortality

Sedentary behavior has been associated with increased risk of several chronic conditions and mortality. However, it is unclear whether physical activity attenuates or even eliminates the detrimental effects of prolonged sitting. A new study examined the associations of sedentary behavior and physical activity with all-cause mortality.

The meta-analysis of trials involving more than 1 million individuals was reported online July 27 in The Lancet. It is one of a special series of papers on physical activity.

The Lancet notes that its first series on physical activity in 2012 concluded that, “physical inactivity is as important a modifiable risk factor for chronic diseases as obesity and tobacco.” The meta-analysis found that 1 hour of moderate-intensity activity, such as brisk walking or riding a bicycle, can offset the health risks of sitting for 8 hours a day. Twenty-five percent of all individuals in the study reported this level of physical activity. The study also discovered that even shorter periods of 25 minutes a day can be beneficial.

For those of us who work by sitting at a desk, it can be very difficult not to sit while we do our jobs.  But, there are still many ways to get moving, like going for a walk during lunch, or even getting up and walking over to an associate to hand them a note instead of sending an email.  There are many ways to get in your physical activity.

According to the researchers, the data from more than a million people is the first meta-analysis to use a harmonized approach to directly compare mortality between people with different levels of sitting time and physical activity. They included 16 studies, with data on 1,005,791 individuals (aged >45 years) from the United States, Western Europe, and Australia.

Researchers divided the study participants into four groups based on their reported levels of physical activity: <5 min/day; 25-35 min/day; 50-60 min/day; and 60-75 min/day.

Researchers noted that, “Among the most active, there was no significant relation between the amount of sitting and mortality rates, suggesting that high physical activity eliminated the increased risk of prolonged sitting on mortality.” But as the amount of physical activity decreased, the risk for premature death increased.

Researchers found prolonged sitting associated with an increase in all-cause mortality, mainly due to cardiovascular disease and cancer (breast, colon, and colorectal), noting that, “A clear dose-response association was observed, with an almost curvilinear augmented risk for all-cause mortality with increased sitting time in combination with lower levels of activity.”

Compared with the referent group (i.e., those sitting <4 h/day and in the most active quartile [>35·5 MET-h per week]), mortality rates during follow-up were 12–59% higher in the two lowest quartiles of physical activity (from HR=1·12, 95% CI 1·08–1·16, for the second lowest quartile of physical activity [<16 MET-h per week] and sitting <4 h/day; to HR=1·59, 1·52–1·66, for the lowest quartile of physical activity [<2·5 MET-h per week] and sitting >8 h/day). Daily sitting time was not associated with increased all-cause mortality in those in the most active quartile of physical activity. Compared with the referent (<4 h of sitting per day and highest quartile of physical activity [>35·5 MET-h per week]), there was no increased risk of mortality during follow-up in those who sat for more than 8 h/day but who also reported >35·5 MET-h per week of activity (HR=1·04; 95% CI 0·99–1·10). By contrast, those who sat the least (<4 h/day) and were in the lowest activity quartile (<2·5 MET-h per week) had a significantly increased risk of dying during follow-up (HR=1·27, 95% CI 1·22–1·31). Six studies had data on TV-viewing time (N=465 450; 43 740 deaths). Watching TV for 3 h or more per day was associated with increased mortality regardless of physical activity, except in the most active quartile, where mortality was significantly increased only in people who watched TV for 5 h/day or more (HR=1·16, 1·05–1·28).

In conclusion, the researchers emphasized that high levels of moderate intensity physical activity (i.e., about 60–75 min per day) seem to eliminate the increased risk of death associated with high sitting time. However, this high activity level attenuates, but does not eliminate the increased risk associated with high TV-viewing time. These results provide further evidence on the benefits of physical activity, particularly in societies where increasing numbers of people have to sit for long hours for work and may also inform future public health recommendations.

In another study published online by JAMA Ophthalmology in August, they found that sedentary behavior may be associated with diabetic retinopathy.  The analysis included 282 participants with diabetes. The average age was 62 years, 29 percent had mild or worse DR, and participants engaged in an average of 522 min/d of SB. The author found that for a 60-min/d increase in SB, participants had 16 percent increased odds of having mild or worse DR; total PA was not associated with DR.  “The plausibility of this positive association between SB and DR may in part be a result of the increased cardiovascular disease risks associated with SB, which in turn may increase the risk of DR.  In order to prove a cause and effect of SB and worsening DR s larger study would be needed.”

Practice Pearls

  • Inactivity is linked to a decreased production of certain hormones.
  • We need to break up periods of sitting for prolonged periods with short bursts of activity.
  • Walking 5 minutes every hour can offset sitting for the other 55 minutes per hour.

Lancet. Published online July 27, 2016. Abstract Editorial How Much Exercise Compensates for Sitting at a Desk Eight Hours A Day?#848 (1)]–[www_diabetesincontrol_com_how_]-[MTExNjQyNDI1NTE1S0]–