Week 11 Diet and Exercise and CVD

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Shon Jonathan Harris
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Week 11 Diet and Exercise and CVD à 2 particularly important cholesterols, LDLs are the bad cholesterols à High LDL in the blood at rest and after a fast would be indicative of a relatively higher

1 Week 11 Diet and Exercise and CVD à 2 particularly important cholesterols, LDLs are the bad cholesterols à High LDL in the blood at rest and after a fast would be indicative of a relatively higher risk of an adverse cardiovascular event downstream à HDL are said to move fat to the gall bladder for excretion, these are the good cholesterols Plasma cholesterol and heart disease Cholesterol has a vital role in manufacturing some vitamins (vitamin D), some hormones and cell membranes. However, the body manufactures all the cholesterol it needs; additional intake in the diet will potentially lead to accumulation of cholesterol in the body. That said, dietary cholesterol intake is not believed to increase plasma [LDL] to the same extent as dietary intake of saturated fat. à While not needed from the diet (we can produce enough for ourselves) it is an important nutrient > hormones, cell membranes etc à Eggs are one of the highest sources of dietary cholesterol > some say if you have high blood cholesterol levels, you should stop consuming so much > this was the 80s > now it is realised that consuming saturated fat is just as, if not more dangerous, for driving up the LDL in the blood. Trans fatty acids have a nasty effect on LDL concentrations in the blood There is a relationship between blood cholesterol concentrations and atherosclerosis (CVD) that has driven public health policy that is, we should reduce our intake of saturated fat in the diet. à Has long been the a relationship between; High sat fat intake <-> high plasma LDL <-> CVD No other blood constituent varies across the World as much as cholesterol. In PNG, TC = 2.6; in Finland, TC = 7.0 mmol.l-1. Total cholesterol seems to be the strongest determinant of CHD risk at a population level. (Coronary Heart Disease) It is dose-related there is no discernible critical level. However, the ratio of HDL:LDL is most informative with respect to CHD risk within a homogenous population. à Relating to the 3 rd point; there is no level that once you hit it you are at greater risk of disease à An individual may have higher than average of LDL conc. Though their ratio of HDL : LDL may be fine > this seems to be related to the overall health and risk Study here about coronary heart disease and calories of fat consumed à There is a relationship between precent of calories of fat in the diet and CHD per 1000 à Sugar - refined carbohydrate can be particularly damaging à Advising to keep levels of sat fat and sugar down in the diet; this is generally in all processed food, so it is generally recommended to avoid processed foods Cholesterol à CHD is a great cause of mortality. The relationship between all cause mortality and plasma cholesterol Saturated fats (and trans fatty acids) consumed in the diet raise cholesterol levels in the blood - to a much greater extent than dietary cholesterol does. Saturated fats are not exclusively derived from animal products. (Palm and coconut oils)

2 So, there epidemiological data have long revealed a relationship between blood cholesterol and mortality. What is the physiological mechanism? Low-density lipoproteins (LDL s) LDL molecules are taken up in the endothelium, where they are oxidized. This oxidation triggers infiltration of other cells and debris and atherosclerosis develops. Low-grade inflammation and oxidative stress plays central role in the series of events leading to LDL oxidation in the endothelium. High circulating glucose and LDL concentrations contribute to the increased inflammatory response and greater oxidative stress. Could antioxidant supplementation reduce LDL oxidation and prevent or slow arthrosclerosis? A meta-analysis by Vivekananthan et al (2003; The Lancet) showed that there is no benefit of vitamin E supplementation on cv disease risk. Moreover, beta carotene supplementation appeared to increase allcause mortality risk. Amorerecentmeta-analysiswith22RCTconfirmedthat antioxidant supplementation has no influence on atherosclerotic events (Katsiki and Manes; 2009; Clinical Nutrition). à There was the thought of taking antioxidants to prevent or slow atherosclerosis and heart disease à The original studies were promising in rats, thought in humans, it seemed to fail. It doesn t seem to have any effect on the development of atherosclerosis High-density lipoproteins (HDLs) HDL removes cholesterol from the peripheries to the liver for disposal. Exercise can increase HDL s but has little influence on LDL s. [HDL] increases with exercise(8-10milesperweek running; Wood et al., 1994) à Hdl concentration doesn t seem to be influenced by diet à It seems that exercise is the best way to push up HDL concentration Kelley and Kelley(2009)have published the results of a meta-analysis (n=29) examining the influence of resistance training on blood lipids. Resistance training can: o Reduce [TC] by 2.7%, reduce [LDL] by 4.6%, reduce [TG] by 6.4% and increase [HDL] by 1.4%. o Ofthe29studiesanalysed, the frequency of RT was either 2 or 3x pw, the reps were between 7-30, exercises ranged between 3-16 and the duration of the training periods lasted 8-78 weeks. à Don t need to know the numbers, just understanding the concepts and support the notion that resistance training can be good for health Graph on risk of cardiovascular events and HDL cholesterol levels à The lower the HDL concentration in the blood the higher the risk à This is similar to the exercise graph where those in the extreme category of exercise, and this graph here, have a greater risk

3 [HDL] should be 1.60 mmol.l-1. A mmol.l-1 increase in [HDL] reduces CHD risk by 2-3%. Smoking decreases [HDL]. HDL levels increase with oestrogen but diet generally has little effect on plasma [HDL]. à A small increase in HDL promotes a significant reduction of the risk of CHD A study on smoking in European men, American men, and Southern European men (Mediterranean) à The Northern European men, and American men have a much greater risk than those on the Mediterranean diet à The steepness represents the rate of death to dying from CHD à Even though there is huge amount of smokers, the Mediterranean diet has a protective affect à The frequency and magnitude of insulin spikes in is thought to be related to vascular dysfunction There is a school of thought that challenges the cause and effect relationship between saturated fat intake and CVD. A number of scientists believe that it is sugar in the diet that is the primary cause of vascular dysfunction. As we will discuss in the diabetes lecture, there is a very close relationship between diabetes and CVD. The reason is that glucose in the blood is associated with oxidative stress, insulin is related to subclinical inflammation and combined, these result in endothelial dysfunction and micro-damage that increases the risks of CVD. Thrombogenesis Platelet aggregation is determined by a complex series of factors. For example, stearic acid (18:0) has no effect on [LDL] but increases clotting. Oleic acid (18:1) is antithrombogenic. à Clotting in the blood > thrombogenesis à The blood can clot too much, a clot in a blood vessel can later travel to the brain (stroke) or heart, etc. Greenland s Indigenous people have traditionally consumed a high fat, high cholesterol diet yet they have low CVD. The reason for this paradox is that they consume high levels of the polyunsaturated fatty acids, particularly the n-3 fatty acids EPA (C20:5) and DHA (22:6) from cold water fish. High blood levels of long-chain n-3 fatty acids are associated with a lower risk of sudden death among men without evidence of prior CVD (Albert et al., 2002). à omega 6 promote clotting (we generally get quite a lot of these through vegetables) à omega 3 balance this as they are anti-clotting à there needs to be a balance between omega 3 and 6 fatty acids!!!! à the benefits of EPA and DHA seem to not just reside with heart disease but also a wide range of health benefits Despite strong epidemiological data and a sound biological explanation for a reduced risk of CVD with increased intake of fish oil, intervention studies have failed to show a relationship. However, there is evidence that it may reduce the risk of CV events with those at particularly high risk of CVD. While trials investigating the relationship between DHA and EPA intake and maintenance of cognitive function and psychological health have bee inconsistent, there is emerging evidence that they may be beneficial. à The weight of evidence is growing, there seems to be sufficient evidence that it plays an important role à High fibre diets don t have that great of an effect

4 Fibre intake and reduced risk of CVD Pectins (fruits) and soluble fibres (oats and barley) reduce cholesterol, but not by much. A very high intake of soluble fibre is necessary to elicit a small effect on [LDL]. Insoluble fibre has no effect on [LDL]. The effect is certainly less than that which occurs in response to changing intakes of saturated fat. à Fibre is very effective of bluntening the BlGlu spike Mechanisms include sterol excretion; removal of bile salts (which are made from cholesterol). High fibre diets make the person feel fuller and can in turn reduce saturated fat intake. Fibreintakeshouldaverageatleast30-40gaday. Giaccoetal.(2009)have recently shown that consumption of 23.1 g/day of cereal fibre reduced [LDL] by 4.3% and TC by 4.9% - in just 3 weeks. Alcohol Alcohol intake mobilizes triglycerides (TGs). The Mediterranean diet that is associated with a relatively low risk of CVD includes red wine. Research has considered whether red wine confers protection against CVD. The French Paradox also... à The French smoke and drink red wine, and their health is generally good Red wine provides a chemical called resveratrol (a polyphenol). Resveratrol levels are higher in red wines produced in harsh climates (from red grapes that have had a stressed life). àit is important not to over emphasis the effect of drinking red wine and resveratrol Berrougui et al. (2009; Atherosclerosis) have attempted to elucidate the mechanisms through which resveratrol reduces the risk of CVD. In test-tube studies, researchers have shown that resveratrol has the potential to reduce LDL oxidation. Whether this translates into meaningful benefits for humans is not clear, though evidence suggests that it may confer benefits. Some studies have shown that it reduces LDL, improves endothelial function and improves ventricular function. à Wine and beer drinkers seem to be different people à Must factor in peoples lifestyle, you can t cherry pick some things from a diet to get the benefit à It is everything in combination NB: resveratrol is believed to be anticarcinogenic and it s influence on colon cancer risk is being investigated. The relation ship between drinking wine (vs beer)and the risk of incurring diseases such as CVD and diabetes has been investigated by Barefoot et al. (2002). Wine drinkers have been found to have more servings of fruit and vegetables each day, consume less cholesterol and saturated fat, consume more fibre and are less likely to smoke when compared to beer drinkers. The research findings related to a protective effect of alcohol on CVD are mixed (and there are biases that often go unreported). Cancer councils recommend abstinence from alcohol (as do the majority of doctors) and it is important that this message does not get clouded by the inconsistent research findings relating protection from CVD by alcohol. It is also worth noting that flavonoids in tea have been associated with a reduced risk of heart disease (Geleijnse et al., 2002). Tea intake (likered wine)is associated with a healthy lifestyle (relatively lean people, low incidence of smoking, healthy diet). Flavonoids protect against LDL oxidation, reduce platelet aggregration and improve vascular function.

5 Hypertension (HT) Hypertension is associated with an increased risk of CVD and stroke. Obesity and alcohol intake are significantly related to HT. Alcohol intake may increase sympathetic outflow, thus increasing peripheral resistance. à As we age the blood vessels lose their elasticity and harden à Heart has to pump harder against this peripheral resistance With regard to salt and HT, the mechanism is less clear. Salt intake is difficult to measure and is generally high in processed foods. 80%ofthesaltconsumedis hidden in processed food. We consume 9-12 g/day this needs to be 5-6 g/day. à Don t need to know numbers for the exam Hypertensives may have a defect in their kidneys ability to clear sodium and water. Sodium may cause vascular reactivity and increase vasoconstriction. It may also raise resting catecholamine levels and renal sympathetic nerve activity. About a 10 mmhg fall in systolic BP is the most hypertensives can expect from a low sodium diet. Also, only 20-40% of hypertensives respond to a reduction in dietary sodium. However, this will reduce the risk of stroke and CHD in the population. à This isn t much and doesn t happen to every body à While this doesn t seem to be that much, at a population level this is actually very effective Fung et al. (2009) examined the influence of the Mediterranean diet on risk of stroke women(aged between 38 and 63 years) in the Nurses Study cohort without a history of CVD and diabetes were followed between 1984 and Relative risk of CVD, stroke and combined fatal cardiovascular disease was assessed. à point of the above is that; no processed food > lower risk of diseases à This is what was thought years ago??? Participants were also assigned a Mediterranean Diet Score (MDS) from dietary records collected six times during the 20-year period. Accounting for confounding variables, those in the top quintile of the MDS had the lowest risk of CVD mortality and stroke. Exercise and hypertension Exercise training (including endurance and resistance training) for those with controlled hypertension can reduce SBP by ~ 10 mmhg. The mechanisms include: Reduced sympathetic response that in turn reduces peripheral vasoconstriction. Increased nitric oxide (NO) production that in turn, increases peripheral vasodilation. In addition to a general improvement in vascular function (peripherally), plasma renin levels may also fall with training and this will improve kidney function. Metabolic Rate Resting metabolic rate (RMR) is the minimum amount of energy required for the maintenance of body functions. It accounts for 60-70% of the total daily energy expenditure. Thus, any intervention that raises RMR has important implications for weight control. A strong relationship exists between lean body mass (LBM) and resting metabolic rate (RMR); trained individuals are characterized by high RMR s. (This is what was though years ago)

This higher RMR in trained individuals has been attributed to alterations in thyroid function, increases in lipolysis, protein synthesis, glycogen synthesis and higher LBM.

6 This higher RMR in trained individuals has been attributed to alterations in thyroid function, increases in lipolysis, protein synthesis, glycogen synthesis and higher LBM. That said, there is little agreement in the research literature that exercise training can increase RMR. à Very few people have consistently shown that muscle can increase RMR Lee et al. (2009; MSSE) recruited 20 healthy males, divided them into two groups and trained one of the groups for 12 weeks. They jogged at 60-80% VO2max for minutes, 3-4 x pw. There was no increase in RMR in the training group but the control group decreased their RMR. The authors speculated that this decrease was seasonal and that the exercise intervention maintained RMR which would have otherwise decreased in the experimental group. Jennings et al. (2009; MSSE) examined whether 6 months of exercise training with previously inactive men (aged > 50 years) who had type II diabetes could increase their RMR. Neither resistance training nor endurance training increased RMR despite increases in strength and VO2max. However, there were trends. Kirk et al. (2009; MSSE) also examined whether 6 months of resistance training with young adults (21 years, BMI = 27) could increase RMR. RT=oneset of nine exercises (3-61RM),3xpw. Each session took 11 minutes to complete. Whole-room indirect calorimetry revealed a significant increase in RMR. à Examining all the studies on training and RMR, there are inconsistencies Thompson et al. (1996) found that RMR falls with dietary manipulation alone (5 MJ/day, low fat) and with dietary manipulation plus exercise. However, the fall in diet alone was greater than diet plus exercise. So, addition of exercise prevents the extent of the fall in RMR. Android vs Gynoid The two individuals in the previous pictures have the same BMI. Android (apple) Pear (gynoid) However, the male (with the android shape) has a much higher risk of CVD, diabetes and dyslipidemia. Visceral fat is higher (e.g. in the liver, heart, pancreas). This leads to metabolic dysfunction of these organs. Android shapes have lower HDL concentrations and higher circulating total triglycerides. à The visceral fat is packed around the organs and seems to be more readily released into the blood stream à This is where problems arise (subcutaneous fat seems a lot less harmful) Increases in visceral fat precede the development of insulin resistance. It may be that deep abdominal (visceral)fat is released more easily into the portal circulation. Visceral fat does appear to be metabolically different to sub-cutaneous fat. Exercise training seems to result in preferential loss of visceral (rather than subcutaneous) fat The International Diabetes Federation has proposed that for males, waist circumference needs to be kept below 94cm; for females, the cut-off is 80cm (Alberti et al., 2009; Circulation). These waist circumference sequate to a BMI of around 25. Waist circumference cut-offs will differ with ethnic group. à Don t need to know numbers

7 Metabolic syndrome The metabolic syndrome is a cluster of the following conditions: o Abdominal obesity o Impaired glucose control o Hypertension o Hyperlipidemia (hyperlipidemia > high blood fat concentration) The combined effects of these conditions is greater than the sum of the risk of each individual condition 34% of adults in developed countries have the metabolic syndrome. à In activity and diet are the main contributors to this The Mediterranean diet In 1980, Keys and colleagues concluded that farmers on Crete consumed very high amounts of dietary fat, yet had the lowest levels of CVD. Key components of the Mediterranean diet include: o Fish (and very little red meat) o Monounsaturated fats from olive oil o Fruit and vegetables o Whole grains, legumes and nuts o Moderate alcohol consumption à It is the interaction between all these things, you can t take one thing from this diet, put it in a pill. It is not clear whether the benefits of the Mediterranean diet are due to some of the individual components or a combined effect. Omega 3 polyunsaturated fats improve blood lipid profiles, reduce inflammation and blood coagulation. Unsaturated fats (olive oil) have phenols that are associated with reduced inflammation and improved endothelial function. Both lead to lower blood pressure. Fruit and vegetables have a wide range of phytochemicals that lead to lower blood pressure. Whole grain food high in fibre, nuts and legumes improve the blood lipid profile and reduce markers of inflammation. à Blood vessel function is v important in avoiding cardiac disease Inflammation Inflammation occurs in the body in response to any disturbance in homeostasis. Uncontrolled-excessive inflammation can result in tissue injury and, for example, to the development of atherosclerosis. Smoking, hypertension, high fat diets, high glucose concentrations cause endothelial cells to bind leukocytes that then secrete chemokines that attract monocytes to enter the intima where they mature into macrophages. à Inflammation in the context of CVD, is considered low grade (not like high temperature), these effect the blood vessels, occurring over a lifetime with poor diet, putting them through low grade inflammation every day An alternative view is that high post-prandial concentrations of glucose and triglycerides generate excess free radicals and these then trigger inflammation and endothelial dysfunction. Either way, high circulating concentrations of glucose and/or fat lead to low-level inflammation and an increased risk of atherosclerosis.

This oxidative stress in the body and the markers that go with it The inflammatory response can cause damage to the blood vessels The principle is most important here Processed food > graph shows the

FMD > flow mediated dilation > how the blood vessel behave, you dont want this to decrease. This suggests impairment post meal.

8 This oxidative stress in the body and the markers that go with it The inflammatory response can cause damage to the blood vessels The principle is most important here Processed food > graph shows the higher the BlGluLevels the greater the oxidative stress in the body (triangle) CRP > c reactive protein systemic marker of inflammation (red box) Nitrotyrosine > measure of oxidative stress (green) FMD > flow mediated dilation > how the blood vessel behave, you dont want this to decrease. This suggests impairment post meal. If it is failing to dilate something is wrong > this is suggesting that there is problems being caused here > even though this is in an extreme case > it goes to show that this adds up over a lifetime This affect lasts for at least 4 hours Reducing the intake of processed food will reduce the inflammatory response. However, exercise will also reduce it via two mechanisms. 1. Exerciselowerspostprandialglucoseconcentrations; a single 90 in bout of moderate-intensity exercise within 2 hr before or after a meal will reduce blood glucose levels and triglyceride levels by up to 50%. 2. Contracting skeletal muscle produces and releases myokines (known also as cytokines). During exercise, interluken-6 (IL-6) is produced by muscles. IL-6 stimulates the appearance of the anti-inflammatory cytokines such as IL-1ra and IL-10 and inhibits the production of the pro-inflammatory cytokine: tumour necrosis factor- alpha (TNF- ). TNF- has been implicated in a variety of diseases, including autoimmune diseases, insulin resistance, and cancer. Thus, IL-6 produces an anti-inflammatory environment as a result of exercise through reducing TNFproduction.

THE SAME EFFECT WAS NOT FOUND WITH SPIRITS 3-5 DRINKS OF SPIRITS PER DAY WAS ASSOCIATED WITH INCREASED MORTALITY

THE SAME EFFECT WAS NOT FOUND WITH SPIRITS 3-5 DRINKS OF SPIRITS PER DAY WAS ASSOCIATED WITH INCREASED MORTALITY ALCOHOL NEGATIVE CORRELATION BETWEEN 1-2 DRINKS PER DAY AND THE INCIDENCE OF CARDIOVASCULAR DISEASE SOME HAVE SHOWN THAT EVEN 3-4 DRINKS PER DAY CAN BE BENEFICIAL - WHILE OTHERS HAVE FOUND IT TO BE HARMFUL