Cardiovascular Disease and Cholesterol
What is Cholesterol?
Cholesterol is a lipid involved in a number of important processes in human body. It is a key component of cell membranes and a precursor for the production of the sex steroid hormones, bile acid and vitamin D. Cholesterol is primarily synthesized by the liver, also regulated / recycled by the liver and transported around the body to cells by lipoproteins.
Is cholesterol the most hyped culprit for cardiovascular disease?
What is Cardiovascular Disease?
Cardiovascular disease is a general term for conditions affecting the heart or blood vessels such as coronary heart disease (CHD), stroke, peripheral arterial disease or aortic disease.
Cardiovascular diseases include
- Coronary heart disease – a disease of the blood vessels supplying the heart muscle
- Peripheral arterial disease – a disease of blood vessels supplying the arms and legs
- Aortic disease – a heart valve disease, the valve between the lower left heart chamber (left ventricle) and the main artery to the body (aorta) doesn’t work properly
- Stroke – stroke occurs when the blood supply to part of brain is interrupted or reduced, preventing brain tissue from getting oxygen and nutrients.
The risk factors for cardiovascular disease
The risk factors are categorized into two basic types. Some risk factors are called modifiable, because one can do something about them. There are other risk factors, called non-modifiable, which one can’t change. However, many non-modifiable risk factors can be controlled and their effect reduced by making changes to lifestyle.
Non-modifiable risk factors are: age, ethnic background, genetic (family history of heart disease), type 1 diabetes and gender.
- Age: The older people are more likely are to develop coronary heart disease.
- Ethnicity: South Asians living in the UK were found to be twice as likely to develop coronary heart disease compared to the rest of the UK population. Also, people from African Caribbean backgrounds were found to be having a higher than average risk of developing high blood pressure.
- Genetic (family history of heart disease): Risk of developing coronary heart disease is increased if one’s father or brother was diagnosed with the disease.
- Type 1 Diabetes: In some research increased risk of premature heart disease in type 1 diabetes has been recognized. Type 1 diabetes is not hereditary (it doesn’t run in the family), but it is genetic (it lives in your genes). Type 1 diabetes is an auto-immune condition. It is not caused by eating the wrong food, or eating too much sugar, or being overweight.
- Gender: Heart disease has long been considered primarily a men’s disease. Although women tend to develop cardiovascular disease about 10 years later in life than men, the outcome for women is often worse.
Modifiable risk factors are: smoking, obesity, hypertension (high blood pressure), abnormal blood lipid levels, poor diet, and sedentary lifestyle.
- Smoking: Smoking is the most preventable risk factor. Smokers have more than twice the risk of developing cardiovascular disease. On average, smoking costs 13 years of life to a male smoker and 14 years to a female smoker. Exposure to smoke — secondhand smoking — increases the risk even for non-smokers.
- Obesity: Obesity is an independent risk factor for the development and progression of coronary heart disease (CHD). Over 80% of patients with CHD are overweight or obese. Weight loss can profoundly influence a number of “major” risk factors including: hypertension, dyslipidemia and insulin resistance/type 2 diabetes mellitus.
- Hypertension (high blood pressure): Blood pressure is the force your blood makes against the walls of your arteries. High blood pressure (hypertension) puts a strain on your heart. Years of high blood pressure can damage arteries, causing them to harden and narrow. This hardening is a primary factor in coronary heart disease, and makes it difficult for the heart to receive oxygenated blood and can lead to CHD.
- Abnormal Blood Lipid levels: Blood lipid levels are modifiable risk factors for CHD. High levels of LDL cholesterol, often called the “bad” cholesterol, are associated with heart disease. LDL cholesterol can stick to artery walls causing the formation of blockages or plaques.
- Poor diet: Diet is an important risk factor in coronary heart disease. Food-related risk factors include obesity, high blood pressure, uncontrolled diabetes and a diet high in saturated fats. A low-saturated fat, high-fiber, high plant food diet can substantially reduce the risk of developing heart disease.
- Sedentary lifestyle: Continuous sitting can lead to negative effects throughout the body, including increased risk for heart disease. Lack of exercise is a known risk for coronary artery disease. This is in part because a sedentary lifestyle increases the risk for diabetes and high blood pressure.
Role of Blood Pressure on CVD
Blood pressure is recorded as two numbers with a ratio, like this: 120/80 mmHg. The top number, called systolic blood pressure, measures the pressure in the arteries when the heart beats. The lower number, called diastolic blood pressure, measures the pressure in the arteries between the heartbeats.
Starting at 115/75 mmHg, cardiovascular disease risk doubles with each increment of 20/10 mmHg throughout the blood pressure range. In a research, evidence indicates a strong association between blood pressure and CHD, which is continuous down to levels of at least 115 mm Hg systolic. Overall, for those 60 to 69 years of age, a 10 mm Hg lower systolic blood pressure is associated with about one-fifth lower risk of a CHD event.
Reducing Blood pressure
There are claims that certain foods reduce blood pressure.
- Garlic – Research is heavily industry funded and findings are mixed/inconclusive.
- Beetroot is shown to reduce blood pressure, specifically systolic blood pressure.
The factors that will make the biggest difference:
- Weight loss
- Not smoking
Is Salt intake to blame for blood pressure?
WHO (World Health Organization) says – “Salt intake of less than 5 grams per day for adults helps to reduce blood pressure and risk of cardiovascular disease, stroke and coronary heart attack. The principal benefit of lowering salt intake is a corresponding reduction in high blood pressure.”
However, there are mixed results in research findings:
- Increasing salt intake from 4g to 15g for 6 days: Did not significantly increase BP in normotensive males (+5.8mmHg)
- Increasing salt intake to 5.5g per day for 4 weeks significantly increased BP – +3.6mmHg Systolic; +2.3mmHg Diastolic
- Reducing salt intake by ~4.4g/day for 4+ weeks significantly reduces systolic & diastolic BP – -5.39mm Hg and -2.82mm Hg in Hypertensive subjects, -2.42mmHg and -1.00mmHg in Normotensive subjects
“Both low sodium intakes and high sodium intakes are associated with increased mortality, consistent with a U-shaped association between sodium intake and health outcomes” – Graudal et al. (2014)
Therefore, the question is – Are high salt intakes causing hypertension or is an unhealthy lifestyle?
A research has found that Sodium / Potassium (Na:K) ratio is more strongly associated with BP outcomes than either Na or K alone in hypertensive individuals – Perez & Chang (2014); Binia et al. (2015)
Cholesterol is a lipid involved in a number of important processes in human body. It is a key component of cell membranes and a precursor for the production of the sex steroid hormones, bile acid and vitamin D. Cholesterol is primarily synthesized by the liver, also regulated/recycled by the liver and transported around the body to cells by lipoproteins.
Cholesterol is found in all the cells in body and is an essential structural component of cell membranes.
- It is synthesized primarily by the liver
- It is regulated/recycled by the liver
- It is transported around the body to cells by lipoproteins
- It is precursor for the production of the sex steroid hormones, bile acid and vitamin D
Different types of Cholesterol
The cholesterol profile includes LDL (bad) cholesterol, HDL (good) cholesterol, triglycerides and total cholesterol.
Total cholesterol is a combination of LDL + HDL. LDL gets its ‘bad’ reputation because it carries cholesterol to cells. There is a strong association between CVD and LDL levels. HDL cholesterol or ‘good cholesterol’ carries cholesterol away from the cells and back to the liver to be recycled or excreted known as Reverse Cholesterol Transport.
- LDL cholesterol LDL cholesterol (low density lipoprotein) contributes to artery blockages (plaques). Most people should aim for an LDL cholesterol level of 100 mg/dL or lower. If you are at very high risk for developing cardiovascular disease, or if you have already had a heart attack, you may need to aim for an LDL level below 70 md/dL.
- HDL cholesterol HDL cholesterol (high density lipoprotein) is a reverse-transport protein; it removes cholesterol from the arteries and takes it to the liver where it can be passed out of the body. High levels of HDL cholesterol lower your risk of developing cardiovascular disease. An HDL level of 60 mg/dL and over is considered excellent, providing you optimal protection.
- Triglyceride is the most common type of fat in the body. A normal triglyceride level is less than 150 mg/dL. Triglycerides increase in the blood with a high fat meal (acute response). Chronically high triglycerides are a risk factor for CVD. Many people who have heart disease or diabetes have high triglyceride levels. There is a strong inverse relationship between triglycerides and HDL cholesterol and also strong links between insulin resistance and elevated triglycerides.
- Total cholesterol Total cholesterol is a measure of LDL cholesterol, HDL cholesterol and other lipids. The desirable level of total cholesterol is less than 200mg/dL.
What is normal?
It’s important to note that healthy cholesterol levels can look different for everyone, depending on other lifestyle factors, medical history, and genetics. But this chart can help give you some general guidelines:
|Cholesterol levels for adults, ages 20 and over|
|Too high or low||>240||High: 160-189
Very high: >190
Very high: >500
Source: US National Library of Medicine
How is Cholesterol Transported?
Cholesterol is transported by complex particles called lipoproteins, which have specific proteins on their surface. These proteins, called apo lipoproteins, have an essential function in the metabolism of lipoproteins. The two most commonly known lipoproteins are low-density lipoproteins (LDL) and high-density lipoproteins (HDL).
Apo lipoproteins, the key components of lipoproteins, play vital roles in the combination and transportation of lipids. apoA, apoB, apoD and apoE are different types of Apo lipoproteins.
|Chylomicrons||Transport dietary triglyceride and cholesterol from intestine to tissue||apoB apoE|
|VLDL||Transports triglyceride from liver to tissues||apoB
|Picks up cholesterol from HDL to become LDL
Intermediary between VLDL and LDL
|LDL||Transports cholesterol to peripheral tissues||apoB|
|HDL||Picks up cholesterol accumulating in blood vessels
Delivers cholesterol to liver
Shuttles apoE in blood
While LDL and total cholesterol are often used as markers of disease risk there are other predictors:
- ApoB:ApoA – The cholesterol balance determined as the apoB/apoA-I ratio has repeatedly been shown to be a better marker than lipids, lipoproteins.
- sdLDL – Small dense low-density lipoprotein (LDL) cholesterol is a type of potentially harmful cholesterol protein that can increase a person’s risk of CVD if one has it in excess.
- oxLDL – One potential marker of MetS risk is oxidized LDL (oxLDL), which is formed when oxidative stress leads to modification of the apoB subunit on LDL cholesterol (LDL).
- TGs – Triglycerides are a type of fat (lipid) found in blood. When you eat, your body converts any calories it doesn’t need to use right away into triglycerides. The triglycerides are stored in your fat cells. When TGs are elevated, lipoprotein metabolism is altered, which increases CVD risk.
- HDL:LDL – LDL cholesterol is often called bad cholesterol. If there is too much LDL cholesterol in the blood, it builds up in the walls of the blood vessels, causing them to narrow and stiffen. A buildup of LDL cholesterol reduces blood flow and can increase the risk of heart attack or stroke. HDL or good cholesterol can move LDL cholesterol from the blood to the liver, which breaks it down for disposal as waste. HDL cholesterol is referred to as good cholesterol because it reduces the level of cholesterol in the blood. Higher HDL levels are linked to a reduced risk of heart attack and heart disease.
- TC:HDL – The total cholesterol to HDL cholesterol ratio can help a person know if they are consuming enough good cholesterol and to limit sources of bad cholesterol. It can be measured by dividing the total cholesterol by the HDL level. Ideally, the ratio should be below 4. The lower this number is, the healthier a person’s cholesterol levels are. Studies suggest that the total cholesterol to HDL ratio is a better marker of the risk of heart disease than LDL cholesterol levels alone.
- non-HDL – Non-HDL cholesterol, as its name implies, simply subtracts your high-density lipoprotein (HDL, or “good”) cholesterol number from your total cholesterol number. So it contains all the “bad” types of cholesterol.
Risk Categories and Target Levels
|Primary Prevention||Secondary Prevention|
|Risk Level||Target||Risk Level||Target|
The CDC guidelines for healthy cholesterol levels are as follows:
- total cholesterol below 200 mg/dL
- LDL cholesterol less than 100 mg/dL
- HDL cholesterol above 40 mg/dL
Atherogenic and anti-atherogenic lipoproteins
Atherogenesis is the process of forming atheromas, plaques in the inner lining (the intima) of arteries. Atherogenic is relating to or causing atherogenesis, to promote the formation of fatty deposits in the arteries.
Anti-atherogenic is the reverse of atherogenic, preventing or inhibiting atherogenesis.
Abbreviations: TG – triglycerides; C – cholesterol; + + increased risk; — reduced risk.
Source: Research Gate
The above diagram shows that there is one single apo-lipoprotein B (apoB) molecule in each large, buoyant or small, dense particle of very-low-density (VLDL), intermediate-density (iDL), and low-density lipoproteins (LDL). Therefore, apoB represents the total number of potentially atherogenic particles. Apo-lipoprotein A-i (apo A-i) is the principal protein component in high-density lipoproteins (HDL) and is responsible for starting reverse cholesterol transport. The balance between apoB and apoA-i is indicative of cardiovascular risk: the greater the ratio, the greater the risk.
Genetic Cholesterol – Familial Hypercholesterolemia
Familial hypercholesterolemia (FH) is a genetic disorder characterized by high cholesterol levels, specifically very high levels of low-density lipoprotein (LDL, “bad cholesterol”), in the blood and early cardiovascular disease.
- Total Cholesterol > 8mmol/L
- LDL-Cholesterol > 4.9mmol/L
Familial hypercholesterolemia is a disorder that is passed down through families. The condition begins at birth and can cause CVD at an early age and is commonly treated with statins.
The Cholesterol Hypothesis
The cholesterol hypothesis, simply stated, is that an elevated blood level of LDL cholesterol is a direct cause of atherosclerosis, a progressive disease where arteries become clogged with plaque. LDL Cholesterol penetrates the endothelium of blood vessels and into the arterial wall behind. This causes an inflammatory process, atherosclerotic plaque is formed. The plaque grows as more cholesterol is deposited, causing damage to the overlying endothelium. Damaged endothelium results in more likely blood clot.
Can we improve blood lipids by manipulating macronutrients?
There are a few places in the world that stand out against the rest of the globe when it comes to freedom free degenerative diseases. One such a place is Kitava, a small island in the Trobriand Islands group of Papua New Guinea where nutritional habits are virtually uninfluenced by Western dietary habits.
Researchers who have studied Kitavans, their lifestyle (including diet) and their exceptional health report that there is practically no acne, diabetes, cardiovascular disease leading to stroke or congestive heart failure, dementia or blood pressure problems among the native Kitavans.
Interestingly, Kitavans do NOT have the optimal blood lipid profiles that Western medicine strives for. They have low HDL levels & high triglycerides, yet they have very low rates of CVD.
Kitavans sources of carbohydrates are very different to the Western sources which COULD be the difference.
Local foods, such as tubers, fresh fruit, coconut and fish, make up the backbone of the Kitavan diet. The most commonly consumed tubers include yam, cassava (aka yucca or manioc), sweet potato (aka kumara) and taro. Common fruit include banana, papaya, guava, pineapple, mango, and water melon. The consumption of Western food is extremely low, with an average Kitavan spending a meagre 3 US dollars per year on Western foods. The intake of dairy products, tea, coffee and alcohol is close to nil, and salt intake is low by Western standards. Also the consumption of oils, margarine, sugar, grains and cereals is low. The overall fat intake is equally low, and most fat consumed is saturated or marine n-3 polyunsaturated fat (omega-3 fat from seafood).
In summary, the Kitavan diet comprises an abundance of foods that have a low glycemic index rating and that are rich in soluble fiber, magnesium, potassium, and omega-3 fatty acids. All of these characteristics may contribute to the exceptional health benefits associated with the Kitavan diet.
Fat Manipulation: Saturated, MUFAs & PUFAs
Replacing SFAs with PUFAs decreases HDL and LDL cholesterol (LDL reduced to a greater extent). HDL: LDL ratio is increased. TC: HDL cholesterol ratio is decreased.
Research has found that effects of PUFAs are stronger than MUFAs.
Replacing SFAs with MUFAs or PUFAs
|Study||Study Intervention||Change in
|Hodson et al.
|Replacing SFAs for n-6 PUFAs
|Didn’t control for:
alcohol (4% EI vs
(303mg vs 174mg)
|Replacing SFAs for MUFAs
|Didn’t control for:
(305mg vs 168mg)
|Bjermo et al.
|High SFAs for 10 weeks (Self
selected diets with some foods
|No change||No change||No change||+4.2% +0.06||Gained 10 weeks 0.8kg over|
|High PUFAs for 10 weeks (Self
selected diets with some foods
|No change||(–4.6%) 0.07||Gained 0.4kg 10 weekso|
|Weech et al.
Vafeiadou et al.
|SFA-rich control diet
Calorie intake was
decreased in the
and PUFA groups
(90 kcal/d), equating
to -2.5 & -1.3 kg,
|Replacement of 8% EI SFAs
|Replacement of 8% EI SFAs
|Piers et al.
(FAT 40%, SFA 24%, MUFA
13%, PUFA 3%)
|2.1kg difference in
weight loss between
(FAT 40%, SFA 11%, MUFA
23%, PUFA 6%)
Effect of Weight Loss on Blood Lipids and CVD Risk
The table below provides evidence that weight loss improves blood lipids.
|Study||Study Intervention||Weight Loss
|Change in TC % (mmol/L)||Change in LDL-C % (mmol/L)||Change in HDL-C % (mmol/L)||Change in TG % (mmol/L)|
|Milsom et al.
|Calorie restricted ~1200, different methods
to achieve calorie deficit in
|Health education program, maintenance on
low Calorie diet and exercise
|4.9||5%||-(24.7% -1.55)||–||–||-(66.9% -0.52)|
|Weiss et al.
|Calorie restriction vs Exercise vs Calorie
Restriction + Exercise (20% deficit);
Intervention until 7% weight-loss achieved
|Wing et al.
|1200-1800 kcal/day (based on body
weight), some meals replaced with shakes,
increased physical activity
|Severe Calorie restriction in obese
individuals for 5 weeks (consumed only
fruit & vegetable juices; high levels of
|12.9||9.9%||-50%||Sig. lower||+20%||decrease Slight|
|Wing et al.
|1200-1800 kcal/day (based on body
weight), some meals replaced with shakes,
increased physical activity
“Dietary replacement of SFA with UFA in metabolically healthy adults with overweight and obesity did not result in statistically significant effects on the modification of lipid profiles”
Replacing Saturated Fat with Carbohydrates
As with dietary cholesterol, there are large inter individual differences in the lipoprotein response to variations in saturated fat intake. Note that some people are more ‘sensitive’ than others.
Research has found that replacement of saturated fat by carbohydrates, particularly refined carbohydrates and added sugars, increases levels of triglyceride and small LDL particles and reduces HDL cholesterol.
CHO restriction (under weight-stable conditions) reduced ApoB, TC:HDL and sdLDL.
Another study found Increasing CHO intake consistently increases TGs.
Saturated vs. Trans Fatty Acids
There is no clear association between higher intake of saturated fats and all cause mortality, CHD, CHD mortality or ischemic stroke in healthy adults.
Consumption of trans-unsaturated fatty acids was associated with a 34% increase in all cause mortality, a 28% increased risk of CHD mortality and a 21% increase in the risk of CHD.
Industrial transfats confer a 30% increase in the risk of CHD events and an 18% increase in the risk of CHD mortality.
No associations found with ruminant transfats i.e. Dairy.
Adhering to the Mediterranean diet reduces CVD mortality risk in US men and women. Greater adherence to the Mediterranean diet associated with reduced fatal & non-fatal CV events in low-risk individuals.
Higher Diet Quality Is Associated with Decreased Risk of All-Cause, Cardiovascular Disease, and Cancer Mortality. However, it is difficult to make strong conclusions due to a lack of dietary standardization.
The impact of alcohol on CVD
Moderate intake (approx. 30g/day)
- Improves HDL cholesterol / ApoA
- Improves Triglycerides
Moderate intakes seem to be
On the basis of published associations between these biomarkers and risk of coronary heart disease 30 g of alcohol a day would cause an estimated reduction of 24.7% in risk of coronary heart disease.
While moderate intake lowers the risk of CVD and is beneficial because of increase in HDL but excessive intake is detrimental.
What other lifestyle changes can help
Fish oils reduce serum triglycerides
- High dose fish oil (3-4g EPA + DHA) can reduce plasma triglycerides by ~30%.
- Primarily due to a reduction in VLDL-TG production & increase in VLDL clearance.
What else do fish oils do?
- Slightly increases LDL and HDL.
- Although mechanistic data has shown the effect of fish oils on decreasing the fractional catabolic rate of HDL apo A-I and HDL apo A-II (stronger effect than statins).
Stress and CVD Risk
Strong associations between job stress/high work demands, daily stresses and CV events/diseases
- Women with high job-related stress had double the risk of myocardial infarction (MI) compared to low job-related stress.
- Elevated stress levels resulted in an odds ratios of 2.5 for myocardial infarction.
Stress reduction RCTs show techniques ‘work’
- Reduced BP, symptoms of anxiety and depression, perceived stress.
In CHD patients, meditation significantly reduced mortality, MI and stroke risk.
Use of Statins
What do statins do?
- Lower LDL Cholesterol
Doctors are currently recommended to prescribe statins for anyone who has a 10 per cent risk of heart disease within a decade.
Under the 2014 NICE guidelines, 11.8 million (37%) adults in England aged 30–84 years, including almost all males >60 years and all females >75 years require statin therapy.
What can we do?
- Weight loss
- Improving dietary quality (e.g. less junk food, processed food, sugar, more veg, variety etc)
- Moderating alcohol intake
- Non-nutritional interventions
- Physical activity, smoking cessation, stress management
- Moderate carbohydrate intake to look after triglyceride levels (This doesn’t mean keto)
- Consider skewed fatty acid profiles – Replacing some saturated fat (if particularly high) with PUFAs may improve LDL and HDL cholesterol
- Encourage egg consumption, especially if dieting.
- Supplement with fish oils due to potential improvements in TGs and HDL-C
- If taking statins, supplement with CoQ10
Striving to drastically manipulate blood lipids through diet is misguided (we are a long way from truly understanding the complexities of this area.
- Lose weight and adopt other healthy behaviors
- Reduce stress!
- Consume a balance of fatty acids (include a fish oil)
Please contact me to learn what we can do through our nutrition and personal training services for kids, teens, adults, elders, athletes and models in Dubai and online across the UAE and around the world to achieve your fat loss, weight loss, muscle gain, strength gain, rehab and figure / physique transformation goals.
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- Cardiovascular diseases (CVDs) https://www.who.int/news-room/fact-sheets/detail/cardiovascular-diseases-(cvds)
- Understanding Your Risk for Heart Disease https://www.ucsfhealth.org/education/understanding-your-risk-for-heart-disease
- Obesity in Coronary Heart Disease: An Unaddressed Behavioral Risk Factor https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5640469/
- Blood pressure and coronary heart disease: a review of the evidence https://pubmed.ncbi.nlm.nih.gov/16222626/
- Salt reduction https://www.who.int/news-room/fact-sheets/detail/salt-reduction
- Cholesterol: Understanding HDL vs. LDL https://www.health.harvard.edu/blog/understanding-cholesterol-hdl-vs-ldl-2018041213608
- The Kitavan Diet: Tubers, Fresh Fruit, Coconut and Fish https://www.healwithfood.org/diet/kitavan-diet-foods.php
Calories in drinks Source.
Abhinav Malhotra is an award-winning personal trainer, coach and sports nutritionist in Dubai, UAE. He also offers online services to clients around the world. A personal trainer par excellence, Abhi has worked with the world’s leading fitness chains, supplement brands and founded his own fitness academy in India. He has achieved successes for many clients from all backgrounds and has trained the Indian Army Rugby Team. He is the first International Kettlebell Sport athlete from India.