Your Road to Wellness

Heart disease

What factors are playing a role in Alzheimer’s, cognitive decline and cardiovascular disease?

Posted by on 9:58 pm Alzheimer’s, Eating, General Health, Get in shape, Health Risk, Heart disease, Stay healthy, Wellness | 0 comments

Alongside oxidative stress and inflammation, altered cholesterol metabolism and hypercholesterolemia also significantly contribute to neuronal damage and to the progression of Alzheimer’s disease (Gamba P, et.al., 2015).

Levels of  oxysterols derived from cholesterol oxidation and inflammatory mediators have been found to be increased in the brains of Alzheimer’s patients (Testa G, et.al., 2016).

Oxysterols, the major component of oxidized LDL is responsible for the increase in endothelial stiffness and is a key step in atherosclerosis development (Shentu TP, et.al., 2012).

When 70 people with mild cognitive impairment were compared with 140 normal individuals, oxysterol levels were significantly higher in the people with mild cognitive impairment (Liu Q, et.al., 2016).

Where do we find oxidized cholesterol?

Oxidized cholesterol are commonly found in foods with high cholesterol content, such as meat, egg yolk and full fatdairy products (Savage GP, et.al., 2002).

Factors known to increase the production of free radicals and therefore oxidized cholesterol in foods are heat, light, radiation, oxygen, moisture and the storage of food at room temperature.

Processes, such as pre-cooking, freeze-drying, dehydration and irradiation, have all been reported to result in increased production of oxidized cholesterol in meats.

What can you do to reduce oxidized cholesterol?

The most obvious way to do it is to avoid the foods that contain the oxidized cholesterol.

The best way to do that is to eat plant based foods, since animal source protein is where you find oxidized cholesterol.

It would also be beneficial to take S-Acetyl Gutathione and Curcumin to reduce free radical damage and inflammation further.

References

Gamba P, Testa G, Gargiulo S, Staurenghi E, Poli G, Leonarduzzi G.Oxidized cholesterol as the driving force behind the development of Alzheimer’s disease. Front Aging Neurosci. 2015 Jun 19;7:119.

Liu Q, An Y, Yu H, Lu Y, Feng L, Wang C, Xiao R.Relationship between oxysterols and mild cognitive impairment in the elderly: a case-control study.Lipids Health Dis. 2016 Oct 10;15(1):177.

Savage GP1, Dutta PC, Rodriguez-Estrada MT, Cholesterol oxides: their occurrence and methods to prevent their generation in foods. Asia Pac J Clin Nutr. 2002;11(1):72-8

Shentu TP, Singh DK, Oh MJ, Sun S, Sadaat L, Makino A, Mazzone T, Subbaiah PV, Cho M, Levitan I.The role of oxysterols in control of endothelial stiffness.J Lipid Res. 2012 Jul;53(7):1348-58.

Testa G, Staurenghi E, Zerbinati C, Gargiulo S, Iuliano L, Giaccone G, Fantò F, Poli G, Leonarduzzi G, Gamba P.Changes in brain oxysterols at different stages of Alzheimer’s disease: Their involvement in neuroinflammation.Redox Biol. 2016 Dec;10:24-33.

 

 

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How and when does cardiovascular disease start?

Posted by on 8:55 pm Anti-aging, Cardiovascular Disease, Cholesterol, Eating, Fat, HDL, Heart disease | 0 comments

 

The clogged pipe analogy is the old, but outdated model of explaining cardiovascular disease which still is used most of the time because of lack of understanding and lack of exposure to research (Rothberg MB, 2013).

According to this model, cholesterol plaque in the arterial walls slowly reduce the opening of the artery, first causing decreased blood flow without symptoms, then it causes angina (chest pain), and eventually it results in an infarction.

Treatments based on this theory include both coronary bypass surgery and angioplasty opening the blood vessel with a stent or a balloon.

While a massive plaque eventually can close up an artery, a heart attack is usually caused by unstable plaque thatmay not be easily detected, but can rupture and form a clot.

This is what happens according to more in depth research.

Low-density lipoprotein (LDL) mainly produced in the liver may infiltrate the vascular endothelium (the inner wall of the blood vessel), where it can initiate a complex inflammatory response. This inflammatory response can lead to arterial remodeling, in which plaque growth within the vessel walls is accommodated by outward enlargement of the vessel.

In that case, large plaques may not reduce the opening of the blood vessel and are therefore hidden from angiography.

These plaques are particularly dangerous both because they are prone to rupture, they are unstable, and because before rupture they do not limit the blood flow and therefore do not induce formation of protective collaterals.

If the blood flow slowly gets restricted as in stable plaque, the body will compensate by making new blood vessels to support the area in need, that’s why stable plaque is less dangerous.

A lot of people apparently have several plaque ruptures in their vascular system without symptoms.These ruptures can heal and is later impossible to detect.

For these reasons it’s very difficult to use available scanning methods as reliable tools to predict  a deadly plaque rupture.

There is however strong evidence that addressing the extent and activity of the atherosclerotic burden and thrombosis-promoting risk factors will improve risk (Arbab-Zadeh A, et.al., 2015).

Oxidized LDL is especially damaging to the endothelium, the inner lining of the blood vessels (Gradinaru D, et al., 2015).

Oxidized LDL cholesterol is associated with early atherosclerosis (Calmarza P, et.al., 2014).

When does atherosclerosis start?

It start at a very young age.

Atherosclerosis varied from 17% in individuals less than 20 years old to 85% in people 50 years old or older (Tuzcu EM, et.al., 2001).

If you have children, this is something to keep in mind. It is very important to have a healthy diet even for a child.

References

Arbab-Zadeh A, Fuster V.The myth of the “vulnerable plaque”: transitioning from a focus on individual lesions to atherosclerotic disease burden for coronary artery disease risk assessment.J Am Coll Cardiol. 2015 Mar 3;65(8):846-855.

Calmarza P1, Trejo JM, Lapresta C, López P,LDL oxidation and its association with carotid artery intima-media thickness and other cardiovascular risk factors in a sample of Spanish general population.Angiology. 2014 Apr;65(4):357-62.

Gradinaru D, Borsa C, Ionescu C, Prada GI,Oxidized LDL and NO synthesis–Biomarkers of endothelial dysfunction and ageing.Mech Ageing Dev. 2015 Nov;151:101-13.

Rothberg MB,Coronary artery disease as clogged pipes: a misconceptual model.Circ Cardiovasc Qual Outcomes. 2013 Jan 1;6(1):129-32.

Tuzcu EM1, Kapadia SR, Tutar E, Ziada KM, Hobbs RE, McCarthy PM, Young JB, Nissen SE.High prevalence of coronary atherosclerosis in asymptomatic teenagers and young adults: evidence from intravascular ultrasound.Circulation. 2001 Jun 5;103(22):2705-10.

 

 

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 Based on the most effective scientific strategies, this program was created to help
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Your Blood Glucose Level after You Eat can Affect Your Risk for Cardiovascular Disease.

Posted by on 11:19 am Bloodsugar, Cardiovascular Disease, Diabetes, Eating, General Health, Glucose, Health, Heart disease | 0 comments

Your blood glucose level after you eat can affect your risk for cardiovascular disease. Several studies show a correlation between blood glucose levels and what happens to your arteries. The most common ways to evaluate the blood glucose metabolism is to measure fasting blood glucose and Hemoglobin A1c (HbA1c). Hemoglobin A1c is usually used to monitor long-term glucose control, 2-3 months.

Image result for blood glucoseMore and more research is, however, documenting the importance of also knowing what the blood glucose level is after a meal, and that is not checked routinely.

In the following study, the participants were divided into 4 groups based on coronary angiography (Sasso FC, et.al., 2004). One group had no significant stenosis (calcification), the other groups had documented disease in 1 and up to 3 vessels. Several tests were performed to evaluate the glucose metabolism, including the glucose and insulin levels after eating.

For patients with a so-called normal glucose tolerance, it was interesting that the most important test correlating with cardiovascular risk was the glucose level after eating, and the next was Hemoglobin A1c.

In patients with coronary artery disease the researchers showed that even with normal Hemoglobin A1c levels, the participants with an abnormal glucose tolerance test (glucose after a meal) had greater progression of coronary artery lesions (Wang H, et.al., 2014).

It was not even a difference in risk between patients with an impaired glucose tolerance and patients who had type 2 diabetes. This shows that you don’t have to have progressed to having diabetes to have an increased risk for cardiovascular disease. Researchers have found that there is a linear relationship between the risk of cardiovascular death and the 2-hour glucose tolerance test (Leiter LA, et.al., 2005).

Image result for cardiovascular disease and glucose level

The 2 -hour glucose tolerance test measures the blood glucose level 2 hours after a test drink has been ingested.

These researchers found increased mortality at an oral 2-hour glucose tolerance test of approximately 90 mg/dl which is well below the level of what type 2 diabetes patients have.

Research is showing us that what we used to think of as normal and good test results are not good enough. That’s probably why we see a lot of people dying from a cardiovascular disease with laboratory values in the normal range.

References
Leiter LA, Ceriello A, Davidson JA, Hanefeld M, Monnier L, Owens DR, Tajima N, Tuomilehto J ; International Prandial Glucose Regulation Study Group. Clin Ther. 2005;27 Suppl B:S42-56.

Sasso FC, Carbonara O, Nasti R, Campana B, Marfella R, Torella M, Nappi G, Torella R, Cozzolino D, Glucose metabolism and coronary heart disease in patients with normal glucose tolerance. JAMA. 2004 Apr 21;291(15):1857-63.

Wang H, Tang Z, Li X, Hu B, Feng B. Angiographic evaluation of the effects of glucose metabolic status on progression of coronary artery lesions in patients with coronary artery disease. J Diabetes. 2014 Nov;6(6):541-6.

 

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Osteoarthritis in women associated with deposits in Arteries

Posted by on 12:33 pm Asthma, Calories, Eating, Energy, Exercise, General Health, General Health, Health Risk, Heart disease, Muscles, Nervous System, Research, Wellness, Women, Womens health | 0 comments

Research sometimes find interesting connections we usually don’t think about.

A study including 3278 women found an association between plaque in the carotid artery and osteoarthritis in the knee and hands in women (Hoeven TA, et.al., 2013).

We know that inflammation is involved in osteoarthritis, even if it is less severe than in rheumatoid arthritis.

We also know that inflammation increases the risk for cardiovascular disease. Inflammation is an important factor in depositing cholesterol and fat into the inner lining of the vascular wall.

 

Another interesting connection found lower magnesium levels in rheumatoid arthritis patients compared to controls (Chavan VU, et.al., 2015).

Lower magnesium levels were also correlated with higher cholesterol and LDL, the so called bad cholesterol, and higher magnesium levels with better HDL cholesterol, the good cholesterol. This was in cases of rheumatoid arthritis.

 

Magnesium has also been found to be inversely associated with osteoarthritis documented on x-rays and joint space narrowing (Zeng C, et.al., 2015).

Glucosamine sulfate another nutritional substance has been used to treat osteoarthritis for many years.

When osteoarthritic chondrocytes (cartilage cells) and glucosamine sulfate were tested in different ways in a culture, it was found that glucosamine sulfate reduced the synthesis of proinflammatory mediators (Largo R, et.al., 2003).

Taking magnesium and glucosamine sulfate could according to this possibly benefit both your cardiovascular system and your joints.

The best form of magnesium is an amino acid chelate like magnesium glycinate.

The most common form of magnesium is magnesium oxide, but that is a gastrointestinal irritant and can give you diarrhea when taken in higher amounts.

 

REFERENCE

Chavan, V. U., Ramavataram, D. V. S. S., Patel, P. A., & Rupani, M. P. (2015). Evaluation of serum magnesium, lipid profile and various biochemical parameters as risk factors of cardiovascular diseases in patients with rheumatoid arthritis. Journal of clinical and diagnostic research: JCDR, 9(4), BC01.

Hoeven, T. A., Kavousi, M., Clockaerts, S., Kerkhof, H. J., van Meurs, J. B., Franco, O., … & Bierma-Zeinstra, S. (2012). Association of atherosclerosis with presence and progression of osteoarthritis: the Rotterdam Study. Annals of the rheumatic diseases, annrheumdis-2011.

Largo R, Alvarez-Soria MA, Díez-Ortego I, Calvo E, Sánchez-Pernaute O, Egido J, Herrero-Beaumont G. Glucosamine inhibits IL-1beta-induced NFkappaB activation in human osteoarthritic chondrocytes.Osteoarthritis Cartilage. 2003 Apr;11(4):290-8.

Zeng C, Li H, Wei J, Yang T, Deng ZH, Yang Y, Zhang Y, Yang TB, Lei GH. Association between Dietary Magnesium Intake and Radiographic Knee Osteoarthritis. PLoS One. 2015 May 26;10(5):e0127666.

 

 

 

 

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Can free radicals clog up your arteries?

Posted by on 9:45 am Heart disease | 0 comments

Yes they can.

Oxidative stress is recognized as an important factor in the creation of cardiovascular disease.

The following research is interesting because the participants were 114 healthy non-smokers without any known atherosclerosis (Ashfaq  S, et al. 2006).

Oxidative stress was estimated by measuring blood levels of glutathione, it’s oxidized form and also their redox state in addition to other factors related to oxidative stress.

The carotid intima-media thickness was measured using ultrasound.

The findings showed that the glutathione redox state, which is a measurement of intracellular oxidative stress, is an independent predictor of the presence of early atherosclerosis in an otherwise healthy population.

What can you do about it?

You can take glutathione to be sure your cells are not depleted.

You have to get glutathione into the cells, and regular glutathione does not get into the cells.

There is only one form of glutathione available which has shown to get into the cells and that is S-Acetyl Glutathione (Cacciatore I, et al. 2010). 


Ashfaq S1, Abramson JL, Jones DP, Rhodes SD, Weintraub WS, Hooper WC, Vaccarino V, Harrison DG, Quyyumi AA. The relationship between plasma levels of oxidized and reduced thiols and early atherosclerosis in healthy adults. J Am Coll Cardiol. 2006 Mar 7;47(5):1005-11. Epub 2006 Feb 9.
Cacciatore I1, Cornacchia C, Pinnen F, Mollica A, Di Stefano A. Prodrug approach for increasing cellular glutathione levels. Molecules. 2010 Mar 3;15(3):1242-64. doi: 10.3390/molecules15031242.

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Glutathione is your primary defense against aging, but regular glutathione is oxidized (destroyed in the stomach) and provides little value. S-Acetyl Glutathione is easily absorbed and provides protection.

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Well proven, but often overlooked cardiovascular risk factor

Posted by on 9:45 am Heart disease | 0 comments

When we think about cardiovascular risk factors, we usually think of high cholesterol.

Cholesterol lowering drugs like statins are the best selling drugs ever and sells for billions every year.

However, high cholesterol is not the only cardiovascular risk factor even if it gets the most attention.

Another risk factor is low grade inflammation even if your doctor may not talk much about that.

There is another well proven risk factor for cardiovascular disease no one usually thinks about, but that does not mean it is not important.

That risk factor is oxidative stress.

The impact of oxidative stress on the cardiovascular system has been investigated.

In on of these studies 114 healthy non-smokers had their carotid intima-media thickness measured using ultrasound (Ashfaq S, et al. 2006).

The intima-media thickness is a measurement of the inner layer of the blood vessel wall and is a way to evaluate atherosclerotic plaque, the buildup of deposits in the blood vessels.

In this study oxidative stress was estimated by measuring blood levels of glutathione which is an important intra cellular antioxidant.

Oxidized glutathione and its so called redox state was also measured.

The redox state is calculated by dividing glutathione with oxidized glutathione and can be looked at as the antioxidant capacity and a measurement of oxidative stress.

Other predictors of intima-media thickness were also measured, these were body mass index, LDL cholesterol, triglycerides, HDL cholesterol and hs-CRP, an inflammatory marker.

The glutathione redox state which is a measurement of intracellular oxidative stress was found to be an independent predictor of early atherosclerosis in an otherwise healthy population.

The body is making glutathione, but we make less as we get older, and we use more since free radical damage to tissue is one of the reasons we age.

Glutathione can be taken as a supplement, but most of the glutathione on the market comes in a form which is not very effective because most of it is oxidized (destroyed) in the stomach.

You need to take glutathione in a form which gets into the cells where it provides protection.

S-Acetyl Glutathione has shown to get into the cells, and it can easily be taken in capsule form.

 

Ashfaq S1, Abramson JL, Jones DP, Rhodes SD, Weintraub WS, Hooper WC, Vaccarino V, Harrison DG, Quyyumi AA. The relationship between plasma levels of oxidized and reduced thiols and early atherosclerosis in healthy adults. J Am Coll Cardiol. 2006 Mar 7;47(5):1005-11. Epub 2006 Feb 9.

 Effective S-Acetyl GlutathioneEffective S-Acetyl Glutathione Transparent

Glutathione is your primary defense against aging, but regular glutathione is oxidized (destroyed in the stomach) and provides little value. S-Acetyl Glutathione is easily absorbed and provides protection.

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