Tag Archive: ldl

Apr 03 2017

LCKL 069 – Biohacks 101 – Fasting – How Fasting Impacts Cardiovascular Disease

If you are dealing with Cardiovascular Disease, High Cholesterol Levels, High Blood Pressure or Inflammation then Fasting has been shown to be very beneficial. This episode will explain why…

SHOWNOTES
  • The impact fasting has on LDL Cholesterol, the different types of LDL cholesterol you may be manufacturing and the dangers of each type of LDL.
  • The impact fasting has on HDL Cholesterol.
  • The impact fasting has on Triglycerides.
  • The impact fasting has on Inflammatory Marker #1 – NLRP3.
  • The impact fasting has on Inflammatory Marker #2 – Homocysteine.
  • The impact fasting has on Inflammatory Marker #3 – IL-6/CRP.
  • The impact fasting has on Inflammatory Marker #4 – Fibrinogen.
  • The impact fasting has on Blood Pressure.
TRANSCRIPT

Unfortunately most of the research that has been done on fasting and cardiovascular disease is that of intermittent fasting or alternate day fasting and not actually extended water fasting. However, I assume that if these results appear after short periods of fasting then they would be even better with extended fasting.

Fasting Lowers Cholesterol LevelsLDL CholesterolHDL CholesterolTriglyceridesNLRP3HomocysteineIL-6/CRPFibrinogenBlood Pressure
  • I have done a podcast specifically on Cholesterol in Episode # 009 so if you would like to learn more about that then it is a good place to start.
  • However, I am going to state a few small overly simplified facts about cholesterol…
    • LDL (Low Density Lipoproteins) are labelled as “bad cholesterol” and high amounts are often linked to cardiovascular disease. However, there are different types of LDL which will determine how dangerous they are. The small, dense LDL is the most dangerous type as they are able to seep through the walls of the arteries and lead to CHD. However, the large, fluffy LDL is much less dangerous as it is unable to get through the walls of the arteries.
    • HDL (High Density Lipoproteins) are labelled as “good cholesterol” and high amounts are often linked to lowered risk of cardiovascular disease. We do not want to see HDL decrease.
    • Triglycerides is the type of fat which is used to store excess energy from our diet and high levels have actually been associated with cardiovascular disease and insulin resistance. Our ultimate aim is to lower triglyceride levels and what is interesting is that it is not actually fats which cause high triglyceride levels but actually carbohydrate consumption. Therefore, by lowering your carbohydrate level you can reduce the risk of triglyceride levels.
  • Alternate day fasting has been found to lower LDL Cholesterol by up to 25% when done for 70 days.
  • Remember that it is the number of small dense LDL which will determine your risk factor for heart disease.
  • IF has been shown to not only decrease total cholesterol, but also the number of small, dense LDL particles.
  • In fact, a research article in the Lipids Health Disease Journal in 2011, titled “Comparison of Effects of Diet versus Exercise weight loss regimens on LDL and HDL particle size in obese adults”, showed that although only exercise actually increased the levels of HDL cholesterol, Alternate Day Fasting actually decreased plasma LDL/decreased the proportion of small LDL particles.
  • Alternate day fasting was also found to increase the proportion of large, fluffy LDL particles in the body.
  • There have also been other studies showing the same thing.
  • Fasting has been shown to have minimal effects on HDL Cholesterol and therefore is not dangerous in any way.

Alternate day fasting has been found to lower Triglycerides by up to 32% when done for 70 days.

  • This is an inflammasome which is involved in the pathogenesis of atherosclerosis.
  • It has been found to increase in the presence of myocardial infarction and its deficiency has been found to improve myocardial infarction.
  • A review titled “The Role of NLRP3 Inflammasome in Cardiovascular Disease” which was published in 2015 by Jasna Ajdukovic came to the conclusion that modulating this particular inflammasome may represent a unique therapeutic strategy to limit cell death and therefore prevent heart failure after a myocardial infarction.
  • This review is amazing and in fact contains so much great information I think I will actually write a blog post on this inflammasome.
  • Well, one of the benefits of fasting is that it has been shown to actually reduce the production of this inflammasome. In fact, a research article in the Journal of Clinical Investigation by Traba et al titled “Fasting and Refeeding differentially regulates NLRP3 inflammasome activation in human subjects” showed that individuals showed less NLRP3 inflammasome activation in the fasted state compared to the fed state. This increase is also linked to an increase in mitochondrial oxidation and free radical production.
  • Homocysteine is a well known amino acid which is an intermediary on the metabolic pathway between methionine and cysteine.
  • They have found that mild to moderate elevation of plasma homocysteine levels increases the risk for development of atherosclerotic vascular disease.
  • Therefore, hyperhomocysteinemia is an independent risk factor for atherosclerosis and people with high levels of homocysteine have been found to have impaired arterial endothelial function.
  • In fact, there was a study in 2007 in the Annals of Nutrition and Metabolism which discussed the positive changes in inflammatory markers that are brought about by intermittent fasting during Ramadam. This showed that levels of homocysteine were reduced during the fast. What is even more interesting is that when they tested the studies for Vitamin B12 and Folate during the fasting period they noticed that the levels were increased substantially, despite not consuming any more food with these nutrients than the non fasting subjects. This is probably the reason homocysteine was lowered.
  • IL-6 is a pro-inflammatory substance that is released from the macrophages and other inflammatory cells which reach the circulation and the liver. When IL-6 levels are high they stimulate an acute phase response in the liver. During this response the liver will release a number of proteins, including CRP.
  • CRP also known as C Reactive Protein is a plasma inflammation marker that has been known to play a role in the development of cardiovascular disease and is an important biomarker which is useful in the prediction of early cardiovascular risk.
  • The Ramadan study just given has shown that fasting not only decreases IL-6 and CRP levels during the fasting period but also for 20 days after completing Ramadam.
  • I believe one of these reasons is because increasing levels of CRP are linked to elevated fasting insulin amongst both lean and obese individuals.
  • This is a blood plasma protein that’s made in your liver and it is one of 13 coagulation factors that are responsible for normal blood clotting.
  • It has been identified as a major independent risk factor for cardiovascular disease due to a number of factors:
    • It contributes to platelet aggregation.
    • Promotes fibrin formation.
    • Major contributor to plasma viscosity.
    • Increased in inflammatory states.
  • In fact, there was a clinical trial that was carried out at a University Hospital with 65 male volunteers with metabolic syndrome during the Ramadam period. They found that after the fast the values of fibrinogen were significantly decreased from 251.7 mg/dL to 239.4 mg/dL.
  • One study titled “Acute effects of short term fasting on blood pressure, circulating noradrenaline and efferent sympathetic nerve activity” by Andersson B et al found that a 48 hour fast showed a reduction in systolic blood pressure from 158 mmHg to 146 mmHg and reduced diastolic blood pressure from 96 mmHg to 89 mmHg.
  • Another study that was done on Ramadam showed that this intermittent fasting caused a drop in both systolic and diastolic blood pressure in normotensive patients.
ADDITIONAL DETAILS
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Please note that this information is not intended for medical purposes or to replace the advice of your medical practitioner. It is for informational purposes only to help guide you on your journey towards optimal wellness.

 

Mar 23 2016

***Research Study*** – Diets with high-fat cheese, high-fat meat, or carbohydrate on cardiovascular risk markers in overweight postmenopausal women: a randomized crossover trial

Cardiovascular Risk: Cheese, Meat or Carbs

“Diets with high-fat cheese, high-fat meat, or carbohydrate on cardiovascular risk markers in overweight postmenopausal women: a randomized crossover trial”

For years we have been told that we must cut Saturated Fat from our diets and increase our “Vegetable Oils”. Well, thankfully research is now showing that this is not the case. But, what type of saturated fats should we be eating?

This study explored the effects of both cheese and meat as sources of Saturated Fatty Acids or Isocaloric replacement with carbohydrates on blood lipids, lipoproteins and fecal excretion of fat.

METHOD

This study consisted of 14 overweight postmenopausal women. Each woman followed 3 separate eating plans (consisting of same number of calories) for a period of 2 weeks each with a 2 week washout period in between (no particular diet).

DIET #1 – A high fat cheese diet;

DIET #2 – A high fat meat diet; and

DIET #3 – A low fat, high carb diet. 

TERMINOLOGY

Apoprotein AI

This is a major protein component of HDL in plasma. It promotes fat efflux including cholesterol from the tissues to the liver for excretion. It also seems to have anti clotting effects. Being a major component of HDL apo A1 helps to clear fats such as cholesterol from the white blood cells within the artery walls, making the cells less likely to become overloaded with fat, transform into foam cells, die and then contribute to progressive atheroma.

Exercise has also been found to increase Apo-AI levels.

Apoprotein B

A form of lipoprotein that is most likely to enter the walls of the arteries. If this number is high, the risk of atherosclerosis will increase and may be a main initiating factor in heart disease. This number has been shown to be a better predictor of cardiovascular disease than LDL cholesterol. Even more than this number, is the ratio between Apo AI and Apo B.

The normal range is 40-125 mg/dL. Less than 100 mg/dL is desirable in low or intermediate risk individuals. In high risk individuals it is wise to get it below 80 mg/dL.

Apo-B is able to be lowered with a low carbohydrate diet and physical exercise.

RESULTS

  • The Cheese Diet caused a 5% higher HDL cholesterol concentration than the Low Fat High Carb Diet;
  • The Cheese Diet caused an 8% higher aporotein AI concentration than the Low Fat High Carb Diet;
  • The Cheese Diet caused a 5% lower apoprotein B than the Low Fat High Carb Diet;
  • The Meat Diet caused an 8% higher HDL cholesterol concentration than the Low Fat High Carb Diet;
  • The Meat Diet caused a 4% higher apoprotein AI concentration than the Low Fat High Carb Diet;
  • Total Cholesterol, LDL cholesterol, apoprotein B and Triacylglycerol were similar with all three diets;
  • Fecal fat excretion was 1.8 and 0.9g higher with the cheese group than the carb and meat groups but the meat diet produced higher fat excretion than the carb group.

CONCLUSIONS

Diets with cheese and meat as primary sources of saturated fatty acids cause higher HDL cholesterol and Apo – 1 and therefore it appears they are both less atherogenic than the low fat high carbohydrate diet.