INTRODUCTION: It is well known that adults are at risk of cardiovascular disease (CVD) due to having obesity and Type 2 Diabetes, but it is now known that children and adolescents are also at risk of premature coronary artery disease and stroke for the same reasons.
According to a new scientific statement from the American Heart Association (AHA) published in the Association’s journal Circulation this past Monday (February 25, 2019) , obesity and severe obesity in childhood and adolescence have been added to the list of conditions that put kids and teenagers at increased risk for premature heart disease, including coronary artery disease (CAD) and stroke and are considered at high risk of cardiovascular disease simply by having Type 2 Diabetes, whether or not they are overweight.
Childhood overweight is defined as a Body Mass Index (BMI) between the 85th to 94th percentile for age and sex, and childhood obesity is defined as having a Body Mass Index (BMI) ≥ 95th percentile for age and sex.
Youth with obesity are now considered at-risk of heart disease and stroke
and those with severe obesity are now considered at moderate risk of heart disease and stroke based on a large-scale study from 2016 that followed 2.3 million people for over 40 years and found the risk of dying from a cardiovascular disease were 2-3 times higher if people’s body weight as adolescents had been in the overweight or obese category, compared to youth with normal weight .
Obesity, specifically the ectopic fat (fat in the organs) is considered an independent risk factor for cardiovascular disease (CVD) and is associated with other CVD risk factors such as high triglycerides, low levels of HDL cholesterol, high blood pressure, high blood sugar (hyperglycemia), insulin resistance, inflammation and oxidative stress.
It Is estimated that in 2014 ~6% of all youth 2 to 19 years old in the United States were severely obese  and 2015 Canadian data indicates that obesity in children aged 5-17 years of age averaged around 12% (14.5% for boys and ~9.5% in girls) .
Given these children are 2-3 times more likely to have premature cardiovascular disease as adults, the time to successfully address their overweight and obesity is when they are still young.
Cardiovascular Disease -a leading cause of death
Cardiovascular disease is the leading cause of death for people of all ages and both genders in the United States  and the second leading cause of death in Canada  and a large percentage of these deaths are entirely preventable with appropriate dietary and lifestyle habit changes whether they are implemented as children, youth or adults.
Proposed Mechanism – inflammation
The American Heart Association scientific statement states that the exact mechanism by which these contribute to cardiovascular disease remains to be fully understood and explained, they believe that the cardiovascular risk is brought about by a combination of insulin resistance and oxidative stress (free radical damage), but that inflammation comes first.
“Insulin resistance, oxidative stress, and
inflammation are linked multidirectionally, but emerging
evidence supports a mechanism by which inflammation
SIDE-NOTE: This idea that inflammation precedes insulin resistance is something I’ve been coming across recently. Some propose that insulin resistance itself may be a protective mechanism against high levels of circulating glucose (sugar) in the blood [a], in much the same way as the ability to produced more and more subcutanous fat (the fat directly under the skin) may be protective against the accumulation of fat around the organs (called visceral fat) or fat in the organs or even the bone (called ectopic fat). That is, excess energy (calories) seen as high levels of glucose in the blood may be the result of storage problems in fat cells (the body’s inability to make new subcutaneous fat cells), and the subsequent overflow of fat may drive excess high glucose production in the liver. a. Nolan CJ, Prentki M, insulin resistance and insulin hypersecretion in the metabolic syndrome and type 2 diabetes: Time for a conceptual framework shift, Diabetes and Vascular Disease Research, Feb 15, 2019
The American Heart Association (AHA) suggests that inflammation may increase cardiovascular risk through a combination of these three factors;
(1) high triglycerides (TG)
(2) low high-density lipoprotein cholesterol (HDL)
(3) high small low-density lipoprotein (LDL) particles (LDL-s)
NOTE: Studies on LDL-particle size indicate that people whose LDL is mostly the small, dense sub-particles have a 3x greater risk of coronary heart disease than those with mostly the large, fluffy sub-particle type, which is thought to be protective.”
The American Heart Association suggests that it’s the inflammatory process itself that triggers insulin resistance as a mechanism to keep blood sugar high in order to meet the needs of an immune system that has become activated, as would occur when the body is fighting a significant infection.
They propose that this process of inflammation leads to;
(1) defective activity of an enzyme that is responsible for breaking down triglycerides (i.e. lipoprotein lipase) which would normally be used by the body as energy or stored in fatty tissue for later use
(2) blocking of normal fat cell creation (adipogenesis)
(3) an increase in triglycerides in order to deal with infectious toxins and
(4) an overproduction of smaller LDL particles* and HDL particles
*The ADA suggests that the formation of small LDL particles may perform some important function in this situation of high inflammation, as small LDL particles can easily penetrate the blood vessels to deliver cholesterol to damaged tissue and that oxidation of these small LDL particles make athlerosclerosis even worse.
The decrease in HDL cholesterol which is frequently seen on a standard cholesterol test (lipid panel) in the context of inflammation is thought to be associated with a decrease in reverse cholesterol transport which promotes the building up of cholesterol in the tissues, where it is used for the synthesis of cortisol for the cell membranes that have become damaged by what the body sees as an ‘infection’.
Recommended Dietary Changes
The AHA recommends different dietary and lifestyle changes for each of the risk factors
The AHA recommends a diet low in simple carbohydrates and added sugars, high in dietary fiber from fruits* and vegetables**, moderate amounts of complex carbohydrates, and high in polyunsaturated*** and monounsaturated fats, without specific restriction of saturated fats.
NOTES: * fructose, the sugar in fruit is a simple carbohydrate and can be a major contributor to high TG. ** there is no distinction between starchy vegetables such as potato and sweet potato (which accounts for a large percentage of overweight children and adult’s ‘vegetable’ servings) and non-starchy vegetables such as leafy greens and cruciferous vegetables, such as broccoli and cauliflower, as well as a whole host of other low carbohydrate non-starchy vegetables. *** it is well established that omega 6 polyunsaturated fats contribute to the inflammation process yet the recommendation doesn’t indicate that there should be a decrease in omega 6 polyunsaturated fats such as from soybean oil, canola oil, etc. and an increase in anti-inflammatory omega 3 fats from fatty fish such as tuna, salmon, sardines, etc even though the paper itself proposes inflammation at the heart of the issue. This makes no sense to me.
Total LDL Cholesterol
Diet high in fiber from fruits* and vegetables**, whole grains, high in polyunsaturated*** and monounsaturated fats, low in saturated
fat and devoid of trans fats.
See Notes above for * , ** and ***.
NOTE: The body of the AHA paper elaborates on the detrimental effect of the small LDL subparticle (LDL-s), yet no such differentiation from total LDL cholesterol (LDL-c) is made in the Dietary Recommendations. Why is that? Particle size of LDL can be established by testing, using Apo B:Apo A ratio (Apo B is a component of lipoproteins involved in atherosclerosis and cardiovascular disease) and by proxy using a TG:HDL ratio. It makes no sense to me that the dietary recommendations focus on total LDL cholesterol when the paper makes it clear that it is the small LDL subparticle that is the risk factor.
Blood glucose (without diagnosis of
Type 1 or Type 2 diabetes)
Low glycemic diet limiting intake of added sugar to ≤5% of total
calories, high in fruits* and vegetables**, encouraging intake of
polyunsaturated*** and monounsaturated fats, and without specific limitation to dietary saturated fats.
See Notes above for * , ** and ***.
Some final thoughts…
The dietary recommendations in this paper that focus on lowering simple carbohydrate and added sugars are very sound, as are recommending moderate amounts of complex carbohydrate and high in monounsaturated fat. However, to me it makes no sense for the AHA to recommend a diet high in fruit when fruit is the primary source of the simple sugar fructose and it also makes no sense to me for the dietary recommendations not to differentiate between starchy vegetables like potatoes, sweet potatoes and corn (which is actually a grain that is counted as a vegetable) that raise blood sugar and the non-starchy vegetables such as salad greens, broccoli and cauliflower and the abundance of other low carbohydrate vegetables.
Furthermore, given that the AHA proposes an inflammatory mechanism at the root of the cardiovascular disease process, it makes no sense to me for the dietary recommendations to fail to differentiate between pro-inflammatory omega 6 polyunsaturated fatty acids (such as those found in soybean and canola oil) and anti-inflammatory omega 3 polyunsaturated fatty acids, such as those found in fatty fish.
Finally, when the body of the paper makes it very clear that it is the small LDL cholesterol subparticle that contributes to athlersclerosis and that oxidization of it in particular is an additional risk factor, why do the dietary recommendations not focus on lowering the small LDL subparticle, rather than total LDL cholesterol?
Eating a lower carbohydrate intake will both reduce triglycerides (TG) and increase high density lipoproteins (HDL), resulting in an improved TG:HDL ratio, which would indicate a reduction in the small, dense LDL subfraction, and reduced risk of cardiovascular disease. Recommending a reduction in saturated fat intake will likely reduce any increase in HDL cholesterol with no consistent evidence that lower total LDL cholesterol will result in lower cardiovascular rates.
On one hand, the paper provides a good explanation about the risks of the small, dense LDL subparticle yet recommends lowering dietary intake of saturated fat, in order to lower total LDL cholesterol.
Why the avoidance of consistent dietary changes that would reduce the small, dense LDL subparticle and increase protective HDL?
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- Statistics Canada. 2015 Canadian Community Health Survey, Measured children and youth body mass index (BMI) (World Health Organization classification), by age group and sex, Canada and provinces, Canadian Community Health Survey.
- Benjamin EJ, Virani SS, Callaway CW et al (on behalf of the American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee). Heart disease and stroke statistics—2018 update: a report from the American Heart Association [published correction appears in Circulation. 2018;137:e493]. Circulation. 2018;137:e67–e492
- Statistics Canada, Leading causes of death, total population, by age group, https://www150.statcan.gc.ca/t1/tbl1/en/tv.action?pid=1310039401