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Cavsor

Cavsor®

FOR HEART HEALTH, SKIN AND HAIR SUPPORT

  • 1 Softgel a day assures the required daily supply of fatty acids (Triple Omega 3-6-9)
  • Supports cardiovascular function and heart health
  • Strengthens the immune and nervous systems
  • Helps to maintain healthy eyes, skin, and hair
  • Made of 100% natural oils in the USA according to GMP standards

 

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WHO NEEDS CAVSOR?

Anyone who wants to have healthy nutrition habits, especially if:

  • You have low consumption of fish products
  • You have documented coronary artery disease
  • You have atherosclerosis, diabetes, ischemic heart disease
  • You have a chronic fatigue syndrome

 

WHY CAVSOR?

  • Cavsor contains scientifically and clinically proven ingredients.
  • Cavsor contains all necessary fatty acids, including essential polyunsaturated fatty acids (PUFA), which enter the body exclusively from external sources and have the ability to reduce the risk of fatal coronary heart disease and sudden cardiac death and are recognized by the Food and Agriculture Organization (FAO) of the United Nations.
  • Cavsor contains an optimal ratio of omega-3 and omega-6 PUFA (1:0.6), which ensures balanced effects of unsaturated fatty acids in the body to match the physiological need for these components.
  • Cavsor contains Eicosapentaenoic acid (EPA), Docosahexaenoic acid (DHA) and vitamin E, which are important for cardiovascular, immune and nervous systems, and eye health.
  • Cavsor is a blend of non-GMO natural oils from borage, flaxseed, and fish. It is manufactured in the USA in accordance with GMP standards from environmentally friendly animal and plant sources, and is a natural product free of chemical agents.
  • Cavsor is produced in an easy-to-swallow softgel. The Cavsor softgel is odor-free and protects its ingredients from oxidation and degradation.

SERVING SIZE:  1 Softgel

SERVINGS PER CONTAINER:  30

Ingredients

Amount Per Serving       

% Daily Value

A proprietary blend of:

Borage Seed Oil, Fish Oil, and Flaxseed Oil yielding

1200 mg

*

n-3 PUFAs:

Alpha-linolenic acid (ALA)

Eicosapentaenoic acid (EPA)

Docosahexaenoic acid (DHA)

178 mg

120 mg

 80 mg

*

n-6 PUFAs:

Linoleic acid (LA)

Gamma-linolenic acid (GLA)

171.6 mg

 72.8 mg

*

 n-9 MUFA:

Oleic acid (OA)

145 mg

*

Vitamin E (as alpha Tocopherol)

 10 IU

33%

Calories

 10

 

Total fat

   1g

2%

* Daily Value not established.

Other ingredients: gelatin, glycerin, purified water

PROPERTIES OF INGREDIENTS

Polyunsaturated fatty acids (PUFAs) have lipid-lowering, anti-arrhythmic, anti-inflammatory, antihypertensive, cardioprotective, and neuroprotective effects. Vitamin E, a powerful antioxidant, protects easily oxidizable monounsaturated fatty acids (MUFAs) and (PUFAs) from oxidation, therefore protecting them from inactivation, which ensures high efficiency of the product.

RECOMMENDED USE

  • Coronary heart disease (including for secondary prevention of myocardial infarction, and in combination with other standard therapies such as statins, antiplatelet agents, beta-blockers, and ACE inhibitors)
  • Dyslipidemia (hyperlipoproteinemia, hypertriglyceridemia); can be combined with statins
  • Arterial hypertension
  • Brain ischemia
  • Peripheral artery disease of the lower extremities (including that accompanied by intermittent claudication)
  • Genetic predisposition to atherosclerosis
  • Thrombosis
  • Obesity (including obesity associated with diabetes)
  • Fatty liver disease, hepatitis of various etiologies
  • Ulcerative colitis, Crohn's disease
  • Allergic bronchopulmonary diseases
  • Rheumatoid arthritis
  • Chronic kidney disease
  • Some skin diseases (psoriasis, eczema), as well as xeroderma (dry skin)
  • Diseases of the nervous system
  • Chronic fatigue
  • Impaired alertness and memory

DIRECTIONS FOR USE

For adults and children over 12: take 1 softgel daily, after a meal, with water. Softgels should be taken without splitting or chewing. For best results, take once daily for at least 3 months.

CONTRAINDICATIONS

Hypersensitivity to one of the components of Cavsor.

WARNINGS

  • If pregnant or nursing, consult your healthcare practitioner before taking this product. This product contains PCBs, a chemical known to the State of California to cause birth defects or other reproductive harm.
  • Contains fish oil.

STORAGE AND PACKAGING

Store in a cool, dry place. Keep out of reach of children.

A bottle contains 30 softgels.

WHAT ARE FATTY ACIDS?

For the human body to function normally, it needs to have a sufficient amount of fatty acids. Fatty acids are important for all organs, skin, brain, blood circulation, immune system function and respiratory system.

Fatty acids are the building blocks of which fat is composed in our bodies and in the food. When digested, our bodies break down fats into fatty acids, which then are absorbed into the blood. Fatty acids help the formation of different molecules in the body, and have many important functions, including:

- energy storage,

- building healthy cells,

- oxygen transport throughout the body.

 

WHAT TYPES OF FATTY ACIDS ARE THERE? WHY DO I NEED ESSENTIAL FATTY ACIDS? 

Of all fatty acids in the human body, 60% are unsaturated and 40% are saturated. Both saturated and unsaturated fatty acids are important for health.

Some unsaturated fatty acids (omega-6 linoleic acid and omega-3 a-linolenic acid), which are deemed essential are not produced by our bodies and can be obtained only from external sources (food or supplements). Some essential fatty acids that are vital for health are rare in average daily diet. Insufficient intake of essential fatty acids may result in various diseases. This is why supplements containing those fatty acids are helpful for the body.

 

WHAT ARE OMEGA 3-6-9 FATTY ACIDS?

Omega-3 fatty acids (ω-3 fatty acids or n-3 fatty acids) are a type of unsaturated fatty acids (polyunsaturated fatty acids). The three types of omega-3 fatty acids involved in human physiology are α-linolenic acid (ALA) (found in plant oils), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) (both commonly found in marine oils). All these components can be found in Cavsor.

Omega-6 fatty acids (ω-6 fatty acids or n-6 fatty acids) are a type of unsaturated fatty acids (polyunsaturated fatty acids).Two of them, Linoleic acid (LA) and Gamma-Linolenic acid (GLA) are the most important for human physiology. They can be found in various types of nuts, seeds and vegetable oils. Cavsor contains Omega-6 fatty acids.

Omega-9 fatty acids (ω−9 fatty acids or n−9 fatty acids) are a family of unsaturated fatty acids (monounsaturated fatty acids). A physiologically important type of Omega-9 fatty acid is Oleic acid (a component of Cavsor), which can be found in olive oil and macadamia oil.

 

WHAT IS EICOSAPENTAENOIC ACID (EPA) AND DOCOSAHEXAENOIC ACID (DHA)? 

Eicosapentaenoic acid (EPA) and Docosahexaenoic acid (DHA) are Omega-3 fatty acids which are important to cardiovascular, immune and nervous systems. Both are components of Cavsor.

 

WHAT IS THE DIFFERENCE BETWEEN CAVSOR AND OTHER FATTY ACIDS SUPPLEMENTS? 

  • Cavsor is a blend of non-GMO natural oils from borage, flaxseed, and fish. This combination provides a rich supply of omega 3, 6, and 9 fatty acids, which are important to cardiovascular, immune and nervous systems, and eye health.
  • Cavsor contains 120 mg of Eicosapentaenoic acid (EPA) and 80mg Docosahexaenoic acid (DHA) -Omega-3 fatty acids which are important to cardiovascular, immune and nervous systems.
  • Cavsor contains some unsaturated fatty acids (omega-6 linoleic acid and omega-3 a-linolenic acid), which are deemed essential, and enter the body exclusively from external sources.
  • Cavsor contains 10 IU of vitamin E, which provides an additional antioxidant effect. Vitamin E, a powerful antioxidant, protects easily oxidizable monounsaturated fatty acids (MUFAs) and (PUFAs) from oxidation, therefore protecting them from inactivation, which ensures high efficiency of the product.

Unlike many other supplements, Cavsor comes in the form of a softgel and has the following advantages:

  • Softgels are easy to swallow and once swallowed, release their contents very quickly.
  • Softgels minimize stomach discomfort.
  • Softgels are ideal for oils as they protect oils from oxidation.
  • Softgels are resistant to temperature fluctuations, making them easy to transport and store.
  • Softgels have the ability to mask odor and unpleasant taste of fish oil.
  • Softgels may enhance the bioavailability of the active ingredients. This is the most widely recognized benefit of softgel technology.

 

CAN I TAKE CAVSOR WITH STATINS? 

Cavsor can be taken with statins for the following reasons:

  1. A number of studies have documented the beneficial cardiovascular effects of an increased consumption of fatty acids that are components of Cavsor. These effects are recognized by the Food and Agriculture Organization (FAO) of the United Nations.
  2. The Japan EPA Lipid Intervention Study (JELIS) investigated the effect of Eicosapentaenoic acid (one of the components of Cavsor) administered in combination with statins in 18,645 patients with hypercholesterolemia. This study revealed a statistically significant (19%) reduction in major coronary events, including myocardial infarction, in patients taking the supplement.
  3. Statins are often used to reduce cholesterol levels. Hypercholesterolemia is a major risk factor for ischemic heart disease. 

 

CAN I TAKE CAVSOR IF I HAVE DIABETES? 

Cavsor contains three n-3 (also called omega-3) polyunsaturated fatty acids (PUFAs), two n-6 (omega-6) and one n-9 (omega-9) PUFAs. Whereas both n-3 and n-6 PUFAs are thought to be beneficial for patients with diabetes, in particular by improving lipid profiles, much more is known about the effects of n-3 than those of n-6 PUFAs. Since fish is a good source of n-3 PUFAs, many studies have assessed the effects of n-3 PUFA intake and/or fish consumption (as a measure n-3 PUFA intake) in diabetic patients or the potential role of n-3 PUFAs in the prevention of diabetes. Although n-3 PUFAs do have beneficial effects in diabetic patients, it should be noted that they do not affect fasting glucose or insulin levels.

 

IS CAVSOR SAFE FOR PATIENTS WITH ISCHEMIC HEART DISEASE OR MYOCARDIAL INFARCTION? 

It is estimated that about 17% of all deaths in men and 10% in women are caused by ischemic heart disease. Ischemic heart disease is the major cause of myocardial infarction (heart attack).

A number of studies have documented the beneficial cardiovascular effects of increased consumption of n-3 (also called omega-3) and n-6 (omega-6) polyunsaturated fatty acids (PUFAs). Cavsor contains three n-3 (including eicosapentaenoic acid, or EPA, and docosahexaenoic acid, or DHA), two n-6, and one n-9 PUFAs.

The beneficial effects of PUFAs, in particular their ability to reduce the risk of fatal ischemic heart disease, are recognized by the Food and Agriculture Organization (FAO) of the United Nations.

 

WHAT IS CHRONIC FATIGUE SYNDROME (CFS)? HOW CAN CAVSOR HELP OVERCOME IT? 

Chronic fatigue syndrome is characterized by persistent exhaustion and most often occurs between the ages of 20–40, although children are sometimes also affected. According to an estimate by the US Centers for Disease Control and Prevention, Chronic Fatigue Syndrome affects more than 1 million people in the USA. The main symptom of the syndrome is fatigue, both physical and mental, which is not alleviated by resting or sleeping. Fatigue may be accompanied by other symptoms, some of which appear to be directly linked to fatigue (inability to concentrate, poor memory, headaches, insomnia), whereas others are not directly related to fatigue (pain in muscles, joints, lymph nodes, or stomach, headaches, sore throat, lymph node enlargement in the neck or armpits).

The exact causes of Chronic Fatigue Syndrome are unknown but may include infection, immunity-related problems, hormonal disturbances, or psychological stress.

In the absence of a definite cure, there are indications that patients with CFS and related conditions have reduced levels of polyunsaturated fatty acids (PUFAs) and that PUFA supplementation may alleviate the CFS symptoms. Taking into account various beneficial health effects of PUFA supplementation, it would make sense for CFS patients to consider taking PUFA supplements such as Cavsor.

 

HOW CAN CAVSOR SUPPORT EYE HEALTH? 

The deficiency of omega-3 polyunsaturated fatty acids in the body has detrimental effects on all parts of the eye and especially on the retina. Therefore, patients with diabetic retinopathy, age-related macular degeneration, dry eye syndrome, and cataract should always include essential lipids and omega fatty acids in their daily diet. The rationale behind supplementation with Cavsor is its balanced content of omega-3, -6 and -9 fatty acids.

Since omega-3 PUFAs are important structural components of cell membranes in the nervous system tissue, including the retina, and are membrane-protective, they are required for the normal functioning of the optic nerve and vision in general.

A clear advantage of Cavsor is the presence of 10 IU of vitamin E, which provides an additional antioxidant effect on eye tissue.

 

HOW LONG CAN I TAKE CAVSOR?

The absence of side effects and safety of long-term intake of Cavsor ingredients have been confirmed by clinical studies. Therefore, there are no time restrictions on regular intake of Cavsor, if consumed at the approved daily dosage of 1 softgel a day.

[more] 

BENEFITS OF TAKING CAVSOR FOR PATIENTS WITH ATHEROSCLEROSIS

A number of studies have documented the beneficial cardiovascular effects of increased consumption of n-3 (also called omega-3) and n-6 (omega-6) polyunsaturated fatty acids (PUFAs)[1,2,3,4]. The beneficial effects of PUFAs, in particular their ability to reduce the risk of fatal coronary heart disease and sudden cardiac death, are recognized by the Food and Agriculture Organization (FAO) of the United Nations [5]. Cavsor contains three n-3 (including eicosapentaenoic acid, or EPA, and docosahexaenoic acid, or DHA), two n-6, and one n-9 PUFAs. 

[endshort]

BENEFITS OF TAKING CAVSOR FOR PATIENTS WITH ATHEROSCLEROSIS

A number of studies have documented the beneficial cardiovascular effects of increased consumption of n-3 (also called omega-3) and n-6 (omega-6) polyunsaturated fatty acids (PUFAs)[1,2,3,4]. The beneficial effects of PUFAs, in particular their ability to reduce the risk of fatal coronary heart disease and sudden cardiac death, are recognized by the Food and Agriculture Organization (FAO) of the United Nations [5]. Cavsor contains three n-3 (including eicosapentaenoic acid, or EPA, and docosahexaenoic acid, or DHA), two n-6, and one n-9 PUFAs. 

 

Atherosclerosis is a major risk factor for cardiovascular disease [6,7,8] and some of the beneficial effects of PUFAs on cardiovascular health are likely due to their antiatherosclerotic effects [1,9], in particular their anti-inflammatory effects. Although atherosclerosis was traditionally considered as a lipid (mainly cholesterol)-associated disease, the evidence accumulated since the late 1990s has resulted in its recognition as an inflammatory disease, in which both adaptive and innate immune responses play a role [10,11]. Therefore, anti-inflammatory agents are now considered promising for prevention and/or treatment of atherosclerosis. In particular, a study currently underway at the University of Oxford (UK) aims to identify the agents able to inhibit the innate immune responses and to use such agents as anti-atherosclerosis drugs [12]. A number of studies have documented the anti-inflammatory effects of n-3 PUFAs, which are likely to underlie their anti-atherosclerotic effects. Some examples of such studies are described below.

 

Effects of PUFAs on the levels of C-reactive protein

Elevated plasma levels of C-reactive protein (CRP), which is an indicator of inflammation, are a well-known risk factor for the development of atherosclerosis. Inhibitors of HMG CoA-reductase inhibitors (statins), which are used as a mainstream therapy to prevent atherosclerosis and cardiovascular disease because they reduce cholesterol levels, also reduce the levels of CRP [13,14]. Several studies suggest that PUFAs reduce the levels of CRP. A study conducted in Denmark, which enrolled 46 patients with chronic renal failure, found that supplementation with 2.4 g n-3 PUFAs daily for 8 weeks reduced the CRP levels by approximately 40%, although this effect did not reach statistical significance due to a small group of examined patients [15].

 

A study conducted in Japan (511 participants aged 21 to 67 years) found that CRP levels tended to be lower in participants taking EPA, DHA, or both, although these relationships did not reach statistical significance [16]. However, when the results in men were analyzed separately, the effects of both n-3 PUFAs and n-6 PUFAs were significant. The findings that the levels of both n-3 PUFAs and n-6 PUFAs are associated reduced CRP levels are corroborated by a more recent study conducted by the French National Institute of Health and Medical Research (INSERM) enrolling 843 participants, which examined the relationship between the intake of n-3 PUFAs, n-6 PUFAs, and vitamin E on CRP levels [17]. The authors found inverse associations between the intake of either n-3 PUFAs or n-6 PUFAs and elevated CRP levels in participants with low intake of vitamin E. Another study by the same team, which included 2031 participants, found a significant positive association between high n-6:n-3 PUFA intake ratio and elevated CRP [17].

 

Effects of PUFAs on the innate immune response

A study conducted in Norway enrolled 563 elderly men with a high risk of atherosclerosis who received n-3 PUFA supplementation or placebo for 3 years [18]. The authors found that the levels of interleukin-18 were significantly reduced by n-3 PUFA and were significantly negatively correlated with the content of EPA and DHA. Interleukin-18 is one of the two early pro-inflammatory mediators produced by a protein complex called inflammasome, which is activated, among many other stimuli, by oxidized low-density lipoprotein and cholesterol crystals and has been implicated in the development of atherosclerosis [19]. Therefore, the findings by Troseid and colleagues suggest one of the possible mechanisms of the ability of n-3 PUFAs to counteract the development of atherosclerosis [18]. 

 

Effects of n-3 PUFAs on stability of atherosclerotic plaques

Plaque ruptures followed by thrombus formation are immediate causes of heart attack and strokes [6]. A number of studies have been devoted to understanding the factors affecting plaque stability [20]. Some of them have found that increased PUFA consumption is associated with improved plaque stability.

 

 A study conducted in the UK enrolled 162 patients who were awaiting carotid endarterectomy [21]. Before surgery, patients were given capsules of fish oil (as a source of n-3 PUFAs), sunflower oil (as a source of n-6 PUFAs), or did not receive any supplement; supplementation lasted for 1.5 months on average. The authors found increased EPA and DHA content in carotid plaques and fewer plaques with signs of inflammation in patients taking n-3 PUFAs in comparison with the control group, whereas n-6 PUFAs had no such effects [21]. The authors concluded that n-3 PUFA intake increased plaque stability, which might underlie the reduced incidence of cardiovascular events associated with n-3 PUFA intake.

 

In line with these results, a later study found that serum content of EPA and DPA was significantly inversely associated with the number of lipid-rich plaques in coronary arteries of patients suspected of having coronary artery disease, and significantly lower n-3 PUFA levels were found in patients diagnosed with acute coronary syndrome [22].

 

Although fish is a good source of PUFAs, it also contains pollutants from seawater, such as mercury, which makes the health benefits of regularly consuming large amounts of fish questionable [3]. In particular, mercury exposure, at least in young adults, is known to increase the risk of diabetes later in life [23]. Although overall the benefits of fish consumption are considered to outweigh the risks, the authors of a study devoted to evaluating the balance between the benefits and risks of high fish consumption advised to avoid certain fish species [3]. Therefore, PUFA–containing supplements such as Cavsor are a good alternative to fish as a source of these essential fatty acids; such supplements are particularly recommended for people with documented coronary artery disease [24].

 

References

  1. Ander, B.P., Dupasquier, C.M., Prociuk, M.A. & Pierce, G.N. Polyunsaturated fatty acids and their effects on cardiovascular disease. Exp Clin Cardiol 8, 164-172 (2003).
  2. Jakobsen, M.U. et al. Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies. Am J Clin Nutr 89, 1425-1432 (2009).
  3. Mozaffarian, D. & Rimm, E.B. Fish intake, contaminants, and human health: evaluating the risks and the benefits. JAMA 296, 1885-1899 (2006).
  4. Mozaffarian, D., Micha, R. & Wallace, S. Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLoS Med 7, e1000252 (2010).
  5. Food and Agriculture Organization of the United Nations. Fats and fatty acids in human nutrition. http://www.fao.org/3/a-i1953e.pdf (2008).
  6. National Health Service, U.K. Atherosclerosis. http://www.nhs.uk/conditions/atherosclerosis/Pages/Introduction.aspx (2014).
  7. National Heart, Lung, and Blood Institute, National Institutes of Health, U.S. Department of Health & Human Services. What is atherosclerosis? http://www.nhlbi.nih.gov/health/health-topics/topics/atherosclerosis (2015).
  8. Inaba, Y., Chen, J.A. & Bergmann, S.R. Carotid plaque, compared with carotid intima-media thickness, more accurately predicts coronary artery disease events: a meta-analysis. Atherosclerosis220, 128-133 (2012).
  9. Grenon, S.M., Hughes-Fulford, M., Rapp, J. & Conte, M.S. Polyunsaturated fatty acids and peripheral artery disease. Vasc Med 17, 51-63 (2012).
  10. Seneviratne, A.N. & Monaco, C. Role of inflammatory cells and toll-like receptors in atherosclerosis. Curr Vasc Pharmacol 13, 146-160 (2015).
  11. Stoll, G. & Bendszus, M. Inflammation and atherosclerosis: novel insights into plaque formation and destabilization. Stroke 37, 1923-1932 (2006).
  12. Monaco, C. Inflammation in atherosclerosis. University of Oxford http://www.kennedy.ox.ac.uk/research/inflammation-in-atherosclerosis (2015).
  13. Strandberg, T.E., Vanhanen, H. & Tikkanen, M.J. Effect of statins on C-reactive protein in patients with coronary artery disease. Lancet 353, 118-119 (1999).
  14. Ridker, P.M. et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. New England J Med 359, 2195-2207 (2008).
  15. Madsen, T., Schmidt, E.B. & Christensen, J.H. The effect of n-3 fatty acids on C-reactive protein levels in patients with chronic renal failure. J Renal Nutr 17, 258-263 (2007).
  16. Poudel-Tandukar, K. et al. Dietary intakes of alpha-linolenic and linoleic acids are inversely associated with serum C-reactive protein levels among Japanese men. Nutr Res 29, 363-370 (2009).
  17. Julia, C. et al. Intakes of PUFAs were inversely associated with plasma C-reactive protein 12 years later in a middle-aged population with vitamin E intake as an effect modifier. J Nutr 143, 1760-1766 (2013).
  18. Troseid, M., Arnesen, H., Hjerkinn, E.M. & Seljeflot, I. Serum levels of interleukin-18 are reduced by diet and n-3 fatty acid intervention in elderly high-risk men. Metab Clin Exp 58, 1543-1549 (2009).
  19. Ozaki, E., Campbell, M. & Doyle, S.L. Targeting the NLRP3 inflammasome in chronic inflammatory diseases: current perspectives. J Inflamm Res 8, 15-27 (2015).
  20. van der Wal, A.C. & Becker, A.E. Atherosclerotic plaque rupture--pathologic basis of plaque stability and instability. Cardiovasc Res 41, 334-344 (1999).
  21. Thies, F. et al. Association of n-3 polyunsaturated fatty acids with stability of atherosclerotic plaques: a randomised controlled trial. Lancet 361, 477-485 (2003).
  22. Amano, T. et al. Impact of omega-3 polyunsaturated fatty acids on coronary plaque instability: an integrated backscatter intravascular ultrasound study. Atherosclerosis 218, 110-116 (2011).
  23. He, K. et al. Mercury exposure in young adulthood and incidence of diabetes later in life: the CARDIA Trace Element Study. Diabetes Care 36, 1584-1589 (2013).
  24. Saita, E., Kondo, K. & Momiyama, Y. Anti-Inflammatory Diet for Atherosclerosis and Coronary Artery Disease: Antioxidant Foods. Clin Med Insights Cardiol 8, 61-65 (2015).

[endmore]

[more]

BENEFITS OF TAKING CAVSOR FOR PATIENTS WITH DIABETES AND FOR THE PREVENTION OF DIABETES

Cavsor contains three n-3 (also called omega-3) polyunsaturated fatty acids (PUFAs), two n-6 (omega-6) and one n-9 (omega-9) PUFAs. Whereas both n-3 and n-6 PUFAs are thought to be beneficial for patients with diabetes, in particular by improving lipid profiles, much more is known about the effects of n-3 than those of n-6 PUFAs [1]. Cavsor contains one short-chain n-3 PUFA (α-linolenic acid) and two long-chain ones (eicosapentaenoic acid, or EPA, and docosahexaenoic acid, or DHA).

[endshort]

BENEFITS OF TAKING CAVSOR FOR PATIENTS WITH DIABETES AND FOR THE PREVENTION OF DIABETES

Cavsor contains three n-3 (also called omega-3) polyunsaturated fatty acids (PUFAs), two n-6 (omega-6) and one n-9 (omega-9) PUFAs. Whereas both n-3 and n-6 PUFAs are thought to be beneficial for patients with diabetes, in particular by improving lipid profiles, much more is known about the effects of n-3 than those of n-6 PUFAs [1]. Cavsor contains one short-chain n-3 PUFA (α-linolenic acid) and two long-chain ones (eicosapentaenoic acid, or EPA, and docosahexaenoic acid, or DHA).

 

Since fish is a good source of n-3 PUFAs, many studies have assessed the effects of n-3 PUFA intake and/or fish consumption (as a measure n-3 PUFA intake) in diabetic patients or the potential role of n-3PUFAs in the prevention of diabetes.

 

Effects of n-3 PUFAs in patients with diabetes

A study conducted at Harvard University examined a potential association between fish consumption or n-3 PUFA intake and the risk of coronary heart disease and total mortality in women diagnosed with type 2 diabetes  The study enrolled 5,103 female diabetic patients who were initially free of cardiovascular disease or cancer. The authors found that an increase in the frequency of fish consumption resulted in a significant reduction in the risk of coronary heart disease and mortality. A similar tendency was observed for n-3 PUFA consumption [2]. 

 

A study conducted in Denmark enrolled 1,014 diabetic patients who previously had a myocardial infarction [3]. Each patient received one of three combinations of n-3 PUFAs or a placebo. The authors found that patients who received a combination of α-linolenic acid, EPA, and DHA (i.e., n-3 PUFAs included in Cavsor) had fewer ventricular arrhythmia–related events and fatal myocardial infarctions in comparison with the placebo group [3].

A forthcoming study conducted in Norway assessed the effects of supplementation with n-3 long-chain PUFAs on the risk of acute myocardial infarction in patients with coronary artery disease and concomitant diabetes (95% type 2 and 5% type 1), pre-diabetes, and those without diabetes (2,378 patients in total, 80% of them men) [4]. The authors found that high n-3 long-chain PUFA consumption was associated with a lower risk of acute myocardial infarction in patients with diabetes but with an increased risk of fatal acute myocardial infarction in those without diabetes. However, potential confounding factors in this study may have been patients’ age, because patients with diabetes were statistically significantly older; they also had a higher body mass index and more often had hypertension [4]. Nevertheless, this study suggests that patients who have coronary artery disease and diabetes at the same time would benefit from taking n-3 PUFA–containing supplements, whereas these supplements should be used with caution in patients with coronary artery disease only. 

 

Although n-3 PUFAs do have beneficial effects in diabetic patients, it should be noted that they do not affect fasting glucose or insulin levels, as revealed by a meta-analysis of 23 clinical trials [5].

 

The role of n-3 PUFAs in the prevention of diabetes

A number of studies have found that consumption of large amounts of n-3 PUFAs is associated with a reduced prevalence of impaired glucose tolerance (which is a risk factor for the development of diabetes [6]) and type 2 diabetes (reviewed by Nettleton and Katz [7]). For example, Adler and coworkers [8] found that consumption of seal oil and salmon, which have a high content of n-3 PUFAs, reduces the risk of glucose intolerance. However, a recent meta-analysis of the data from nine clinical studies (438,214 participants in total) on the effect of fish or n-3 PUFA consumption on the incidence of diabetes did not find any overall effect, although the authors found an inverse association between fish consumption and the risk of diabetes in three studies conducted in Asia (Japan and China) [9]. The authors suggested that a possible reason for the difference between Eastern and Western populations may be explained by a difference in the prevalent ways of cooking fish: whereas in Asia fish is mainly consumed raw, boiled, or steamed, in Western countries it is often fried, which may reduce the content of n-3 long-chain PUFAs and increase the content of trans-fatty acids and lipid oxidation products, which are known to increase the risk of diabetes [9]. Another possible explanation could be that fish consumption in Eastern countries is higher than in Western countries, resulting in a higher n-3 long-chain PUFA intake [9]. If the latter explanation is correct, then n-3 long-chain PUFA intake via food supplements such as Cavsor could be expected to reduce the risk of development of diabetes in Western populations as well.

 

The beneficial effect of n-3 PUFA intake (as assessed from fish consumption) on the prevention of type 2 diabetes in Asian but not Western populations has also been revealed by an independent meta-analysis, which included 24 studies that enrolled 545,275 participants, including 24,509 patients with type 2 diabetes [10]. The authors also found that tissue levels of n-3 PUFAs in patients with diabetes were significantly lower than those in healthy participants in Asian populations but not in Western populations, and suggested that genetic differences and gene–diet interaction may play a role. However, despite the several possible explanations suggested, reasons for this difference between Asians and Westerners remain to be established.

 

The meta-analyses by Xun et al. [9] and Zheng et al. [10] reflect the general tendency mentioned above: many studies have assessed fish consumption as a proxy for the consumption of n-3 PUFAs. In addition to possible uncertainties because of differences in fish species consumed or different ways of cooking fish, another confounding factor in such studies may be the presence of pollutants in fish, for example mercury, which is a well-known toxin [11]. To address the uncertainties about the effect of n-3 PUFAs on the risk of type 2 diabetes, a study conducted in Finland, which lasted for almost two decades and was published in 2014 [11], directly measured the actual serum levels of n-3 PUFAs in addition to assessing their intake, and also controlled for the presence of mercury in hair. This study enrolled 2,212 middle-aged and older Finnish men, of whom 422 developed type 2 diabetes over the observation period (19.3 years). The authors found that the combined content of EPA, DHA, and docosapentaenoic acid was statistically significantly associated with a lower long-term risk of type 2 diabetes, whereas mercury had no effect [11]. Therefore, unlike studies using fish consumption as a measure of n-3 PUFA intake, this study has established a link between n-3 PUFA levels and reduced risk of type 2 diabetes also in a Western population, which warrants the use of n-3 PUFA–containing supplements (such as Cavsor) by Westerners, regardless of the level of fish consumption.

 

Whereas most studies have assessed the effect of n-3 PUFA on the most prevalent type 2 diabetes or combined the data for type 1 and type 2 diabetes, a recent study has reported that type 1 diabetes reduces availability of n-3 PUFA, in particular n-3 long-chain PUFA, at least in children with concomitant celiac disease [12]. Whereas the cause–effect relationship between type 1 diabetes and the content of n-3 PUFAs remains to be elucidated, this finding suggests that n-3 PUFA supplementation might benefit type 1 diabetes patients or be useful for the prevention of this form of diabetes as well.

 

As mentioned above, fish is a good source of n-3 PUFAs; however it also contains pollutants from seawater, such as mercury, which makes the health benefits of regularly consuming large amounts of fish questionable. In particular, mercury exposure, at least in young adults, is known to increase the risk of diabetes later in life [13]. Therefore, n-3 PUFA–containing supplements such as Cavsor are a good alternative to fish as a source of these essential fatty acids.

 

References

  1. Jeppesen, C., Schiller, K. & Schulze, M.B. Omega-3 and omega-6 fatty acids and type 2 diabetes. Curr Diab Rep 13, 279-288 (2013).
  2. Hu, F.B., Cho, E., Rexrode, K.M., Albert, C.M. & Manson, J.E. Fish and long-chain omega-3 fatty acid intake and risk of coronary heart disease and total mortality in diabetic women. Circulation 107, 1852-1857 (2003).
  3. Kromhout, D. et al. n-3 fatty acids, ventricular arrhythmia-related events, and fatal myocardial infarction in postmyocardial infarction patients with diabetes. Diabetes Care 34, 2515-2520 (2011).
  4. Strand, E. et al. Dietary intake of n-3 long-chain polyunsaturated fatty acids and risk of myocardial infarction in coronary artery disease patients with or without diabetes mellitus: a prospective cohort study. BMC Med 11, 216 (2013).
  5. Hartweg, J. et al. Omega-3 polyunsaturated fatty acids (PUFA) for type 2 diabetes mellitus. Cochrane Database Syst Rev, CD003205 (2008).
  6. http://www.diabetes.co.uk/impaired-glucose-tolerance.html.
  7. Nettleton, J.A. & Katz, R. n-3 long-chain polyunsaturated fatty acids in type 2 diabetes: a review. J Am Diet Assoc 105, 428-440 (2005).
  8. Adler, A.I., Boyko, E.J., Schraer, C.D. & Murphy, N.J. Lower prevalence of impaired glucose tolerance and diabetes associated with daily seal oil or salmon consumption among Alaska Natives. Diabetes Care 17, 1498-1501 (1994).
  9. Xun, P. & He, K. Fish Consumption and Incidence of Diabetes: meta-analysis of data from 438,000 individuals in 12 independent prospective cohorts with an average 11-year follow-up. Diabetes Care35, 930-938 (2012).
  10. Zheng, J.S., Huang, T., Yang, J., Fu, Y.Q. & Li, D. Marine N-3 polyunsaturated fatty acids are inversely associated with risk of type 2 diabetes in Asians: a systematic review and meta-analysis. PLoS One 7, e44525 (2012).
  11. Virtanen, J.K., Mursu, J., Voutilainen, S., Uusitupa, M. & Tuomainen, T.P. Serum omega-3 polyunsaturated fatty acids and risk of incident type 2 diabetes in men: the Kuopio Ischemic Heart Disease Risk Factor study. Diabetes Care 37, 189-196 (2014).
  12. Tarnok, A., Marosvolgyi, T., Szabo, E., Gyorei, E. & Decsi, T. Low n-3 long-chain polyunsaturated fatty acids in newly diagnosed celiac disease in children with preexisting type 1 diabetes mellitus. J Pediatr Gastroenterol Nutr 60, 255-258 (2015).
  13. He, K. et al. Mercury exposure in young adulthood and incidence of diabetes later in life: the CARDIA Trace Element Study. Diabetes Care 36, 1584-1589 (2013).

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BENEFITS OF TAKING CAVSOR FOR PATIENTS WITH ISCHEMIC HEART DISEASE FOR SECONDARY PROPHYLAXIS OF MYOCARDIAL INFARCTION IN COMBINATION WITH STANDARD TREATMENTS (STATINS, ANTIPLATELET PRODUCTS, BETA-BLOCKERS, AND ACE INHIBITORS)

Ischemic heart disease (also called coronary heart disease or coronary artery disease) is caused by the narrowing of the coronary arteries, which supply the heart muscle with oxygen-rich blood; the narrowing, in turn, is caused by atherosclerosis, i.e. the build-up of fatty material (atheroma) in the artery walls [1, 2, 3]. Thus, ischemic heart disease is a direct consequence of atherosclerosis, and the two terms are sometimes considered synonymous [1]. It is estimated that about 17% of all deaths in men and 10% in women are caused by ischemic heart disease [2]. Ischemic heart disease is the major cause of myocardial infarction (heart attack) [4].

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BENEFITS OF TAKING CAVSOR FOR PATIENTS WITH ISCHEMIC HEART DISEASE FOR SECONDARY PROPHYLAXIS OF MYOCARDIAL INFARCTION IN COMBINATION WITH STANDARD TREATMENTS (STATINS, ANTIPLATELET PRODUCTS, BETA-BLOCKERS, AND ACE INHIBITORS)

Ischemic heart disease (also called coronary heart disease or coronary artery disease) is caused by the narrowing of the coronary arteries, which supply the heart muscle with oxygen-rich blood; the narrowing, in turn, is caused by atherosclerosis, i.e. the build-up of fatty material (atheroma) in the artery walls [1, 2, 3]. Thus, ischemic heart disease is a direct consequence of atherosclerosis, and the two terms are sometimes considered synonymous [1]. It is estimated that about 17% of all deaths in men and 10% in women are caused by ischemic heart disease [2]. Ischemic heart disease is the major cause of myocardial infarction (heart attack) [4].

 

A number of studies have documented the beneficial cardiovascular effects of increased consumption of n-3 (also called omega-3) and n-6 (omega-6) polyunsaturated fatty acids (PUFAs) 5, [6, 7, 8]. The beneficial effects of PUFAs, in particular their ability to reduce the risk of fatal ischemic heart disease, are recognized by the Food and Agriculture Organization (FAO) of the United Nations [9]. Cavsor contains three n-3 (including eicosapentaenoic acid, or EPA, and docosahexaenoic acid, or DHA), two n-6, and one n-9 PUFAs. 

 

Although atherosclerosis was traditionally considered as a lipid (mainly cholesterol)-associated disease, the evidence accumulated since the late 1990s has resulted in its recognition as an inflammatory disease, in which both adaptive and innate immune responses play a role [10, 11]. For beneficial effects of PUFAs for patients with atherosclerosis that are due to their anti-inflammatory action. This article considers the available evidence regarding the effects of PUFA intake on secondary prophylaxis of myocardial infarction, i.e. prophylaxis in patients who already have ischemic heart disease and may have already had myocardial infarction.

 

Prophylaxis of myocardial infarction in patients with diabetes

A study conducted in Norway assessed the effects of supplementation with n-3 long-chain PUFAs on the risk of acute myocardial infarction in patients with ischemic heart disease and concomitant diabetes (95% type 2 and 5% type 1), pre-diabetes, and those without diabetes (2378 patients in total, 80% of them men) [12]. The authors found that high n-3 long-chain PUFA consumption was associated with a lower risk of acute myocardial infarction in patients with diabetes but with an increased risk of fatal acute myocardial infarction in those without diabetes. However, a potential confounding factor in this study may have been patients’ age, because patients with diabetes were statistically significantly older; they also had higher body mass index and more often had hypertension [12]. Nevertheless, this study suggests that patients who have ischemic heart disease and diabetes at the same time would benefit from taking n-3 PUFA–containing supplements.

 

A study conducted in Denmark enrolled 1014 diabetic patients who previously had myocardial infarction [13]. Each patient received one of three combinations of n-3 PUFAs or placebo. The authors found that patients who received a combination of α-linolenic acid (ALA), EPA, and DHA (i.e., n-3 PUFAs included in Cavsor) had fewer ventricular arrhythmia–related events and fatal myocardial infarctions in comparison with the placebo group [13].

 

Prophylaxis in patients with hypercholesterolemia undergoing statin treatment. Hypercholesterolemia (a high level of cholesterol in the blood) is a major risk factor for ischemic heart disease [2]. Statins, the inhibitors of HMG-CoA reductase, an enzyme necessary for cholesterol synthesis, are often used to reduce cholesterol levels. EPA (one of the components of Cavsor) has also been reported to reduce cholesterol levels in patients with hypercholesterolemia [14]; thus, one could assume that a combination of statin therapy with supplements containing n-3 PUFAs might be more efficient in reducing the risks associated with ischemic heart disease than each treatment alone. Another rationale for combining statins and n-3 PUFA supplementation is that some statins may reduce n-3 PUFA levels [15, 16], and this side effect appears to be associated with the increased volume of atherosclerotic plaques [17] and with the residual risk of cardiovascular events despite statin therapy [16]. In addition, hypertriglyceridemia (increased levels of triglycerides) is an independent risk factor for mortality in patients with ischemic heart disease [18], and n-3 PUFAs but not statin treatment reduce triglyceride levels [19]. 

 

A randomized, open-label, blind study, named the Japan EPA Lipid Intervention Study (JELIS), was designed to investigate the effect of EPA (1.8 g daily) administered in combination with statins in patients with hypercholesterolemia [20]. This study, which included as many as 18,645 patients in total, found a statistically significant 19% reduction in major coronary events, including myocardial infarction, in patients taking the supplement [21]. Further analysis of the data for 1,050 patients with prior myocardial infarction showed that EPA administration significantly reduced the incidence of major coronary events (by approximately 25%) [22]. The results of this study and the above considerations indicate that supplements containing n-3 PUFAs should be beneficial for patients with ischemic heart disease undergoing statin therapy.

 

Prophylaxis in patients undergoing antiplatelet (antithrombotic) treatment

Treatment with antiplatelet (antithrombotic) agents such as aspirin and/or clopidogrel is widely used in patients with ischemic heart disease [23]; for example, the use of aspirin moderately reduces the risk of myocardial infarction (either fatal or non-fatal) in such patients [24]. The OMEGA-PCI (Omega-3 Fatty Acids After PCI to Modify Responsiveness to Dual Antiplatelet Therapy) trial, a prospective, double-blind, placebo-controlled, randomized study that included patients undergoing aspirin plus clopidogrel therapy, found that supplementation with n-3 PUFAs (1g daily for 4 weeks) significantly potentiated platelet response to antiplatelet treatment [25]. In a follow-up study, the authors found that n-3 PUFA supplementation in these patients also significantly reduced thrombin formation, attenuated oxidative stress and favorably changed fibrin clot properties [26].

 

Supplementation with n-3 PUFAs in patients treated with beta-blockers and ACE inhibitors

Beta-blockers (β-adrenoceptor–blocking agents) [27, 28] and angiotensin-converting enzyme (ACE) inhibitors [29] have long been used in patients with various cardiovascular diseases, including ischemic heart disease; beta-blockers improve the survival of these patients. A recent study conducted in Finland (985 participants) suggested an inverse association between the level of the n-3 PUFA docosapentaenoic acid (DPA) and the level the natriuretic peptide NT-proBNP (natriuretic peptides are considered as markers for cardiovascular disease), particularly among patients treated with beta-blockers [30]; this observation suggests a possible synergistic effect of treatment with beta-blockers and n-3 PUFA supplementation. However, a large study conducted in Italy (GISSI-Prevenzione; 9630 patients with prior myocardial infarction) found that n-3 PUFA supplementation significantly reduced mortality in a manner independent of the effects of either beta-blockers or ACE inhibitors [31]. Curiously, PUFAs, especially EPA, ALA, and DHA (all of which are included in Cavsor) have been reported to suppress ACE activity in isolated leukocytes [32] and thus have been hypothesized to act as endogenous ACE inhibitors [33]. Whether n-3 PUFAs act synergistically with or independently from beta-blockers and ACE inhibitors, these data suggest that it makes sense to use them in combination with these well-established therapies.

 

References

  1. National Heart, Lung, and Blood Institute, National Institutes of Health, U.S. Department of Health & Human Services. What is coronary heart disease? https://www.nhlbi.nih.gov/health/health-topics/topics/cad (2015).
  1. National Health Service, U.K. Coronary heart disease. http://www.nhs.uk/Conditions/Coronary-heart-disease/Pages/Introduction.aspx (2014).
  2. British Heart Foundation. Coronary heart disease. https://www.bhf.org.uk/heart-health/conditions/coronary-heart-disease.aspx (2016).
  3. British Heart Foundation. Heart attack. https://www.bhf.org.uk/heart-health/conditions/heart-attack(2016).
  4. Ander, B.P., Dupasquier, C.M., Prociuk, M.A. & Pierce, G.N. Polyunsaturated fatty acids and their effects on cardiovascular disease. Exp Clin Cardiol 8, 164-172 (2003).
  5. Jakobsen, M.U. et al. Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies. Am J Clin Nutr 89, 1425-1432 (2009).
  6. Mozaffarian, D. & Rimm, E.B. Fish intake, contaminants, and human health: evaluating the risks and the benefits. JAMA 296, 1885-1899 (2006).
  7. Mozaffarian, D., Micha, R. & Wallace, S. Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLoS Med 7, e1000252 (2010).
  8. Food and Agriculture Organization of the United Nations. Fats and fatty acids in human nutrition. http://www.fao.org/3/a-i1953e.pdf (2008).
  9. Seneviratne, A.N. & Monaco, C. Role of inflammatory cells and toll-like receptors in atherosclerosis. Curr Vasc Pharmacol 13, 146-160 (2015).
  10. Stoll, G. & Bendszus, M. Inflammation and atherosclerosis: novel insights into plaque formation and destabilization. Stroke 37, 1923-1932 (2006).
  11. Strand, E. et al. Dietary intake of n-3 long-chain polyunsaturated fatty acids and risk of myocardial infarction in coronary artery disease patients with or without diabetes mellitus: a prospective cohort study. BMC Med 11, 216 (2013).
  12. Kromhout, D. et al. n-3 fatty acids, ventricular arrhythmia-related events, and fatal myocardial infarction in postmyocardial infarction patients with diabetes. Diabetes Care 34, 2515-2520 (2011).
  13. Nozaki, S. et al. Effects of purified eicosapentaenoic acid ethyl ester on plasma lipoproteins in primary hypercholesterolemia. Int J Vitamin Nutr Res 62, 256-260 (1992).
  14. Nozue, T. et al. Effects of statins on serum n-3 to n-6 polyunsaturated fatty acid ratios in patients with coronary artery disease. J Cardiovasc Pharmacol Therapeutics 18, 320-326 (2013).
  15. Kurisu, S. et al. Effects of lipid-lowering therapy with strong statin on serum polyunsaturated fatty acid levels in patients with coronary artery disease. Heart Vessels 28, 34-38 (2013).
  16. Nozue, T. et al. Comparison of effects of serum n-3 to n-6 polyunsaturated fatty acid ratios on coronary atherosclerosis in patients treated with pitavastatin or pravastatin undergoing percutaneous coronary intervention. Am J Cardiol 111, 1570-1575 (2013).
  17. Klempfner, R. et al. Elevated triglyceride level is independently associated with increased all-cause mortality in patients with established coronary heart disease: Twenty-two-year follow-up of the bezafibrate infarction prevention study and registry. Circ Cardiovasc Qual Outcomes 9, 100-108 (2016).
  18. Tomei, R. et al. Efficacy and tolerability of simvastatin and omega-3 fatty acid combination in patients with coronary disease, hypercholesterolemia and hypertriglyceridemia. Cardiologia 38, 773-778 (1993).
  19. Yokoyama, M. & Origasa, H. Effects of eicosapentaenoic acid on cardiovascular events in Japanese patients with hypercholesterolemia: rationale, design, and baseline characteristics of the Japan EPA Lipid Intervention Study (JELIS). Am Heart J 146, 613-620 (2003).
  20. Yokoyama, M. et al. Effects of eicosapentaenoic acid on major coronary events in hypercholesterolemic patients (JELIS): a randomised open-label, blinded endpoint analysis. Lancet369, 1090-1098 (2007).
  21. Matsuzaki, M. et al. Incremental effects of eicosapentaenoic acid on cardiovascular events in statin-treated patients with coronary artery disease. Circ J 73, 1283-1290 (2009).
  22. Schulman, S. & Spencer, F.A. Antithrombotic drugs in coronary artery disease: risk benefit ratio and bleeding. J Thromb Haemost 8, 641-650 (2010).
  23. Baigent, C. et al. Aspirin in the primary and secondary prevention of vascular disease: collaborative meta-analysis of individual participant data from randomised trials. Lancet 373, 1849-1860 (2009).
  24. Gajos, G., Rostoff, P., Undas, A. & Piwowarska, W. Effects of polyunsaturated omega-3 fatty acids on responsiveness to dual antiplatelet therapy in patients undergoing percutaneous coronary intervention: the OMEGA-PCI (OMEGA-3 fatty acids after pci to modify responsiveness to dual antiplatelet therapy) study. J Am Coll Cardiol 55, 1671-1678 (2010).
  25. Gajos, G. et al. Reduced thrombin formation and altered fibrin clot properties induced by polyunsaturated omega-3 fatty acids on top of dual antiplatelet therapy in patients undergoing percutaneous coronary intervention (OMEGA-PCI clot). Arterioscler Thromb Vasc Biol 31, 1696-1702 (2011).
  26. Elgendy, I.Y., Mahmoud, A. & Conti, C.R. Beta-blockers in the management of coronary artery disease: are we on the verge of a new paradigm shift? Recent Pat Cardiovasc Drug Discov 9, 11-21 (2014).
  27. Boudonas, G.E. beta-Blockers in coronary artery disease management. Hippokratia 14, 231-235 (2010).
  28. Donnelly, R. & Manning, G. Angiotensin-converting enzyme inhibitors and coronary heart disease prevention. J Renin Angiotensin Aldosterone Syst. 8, 13-22 (2007).
  29. Daneshmand, R., Kurl, S., Tuomainen, T.P. & Virtanen, J.K. Associations of serum n-3 and n-6 polyunsaturated fatty acids with plasma natriuretic peptides. Eur J Clin Nutr (2016).
  30. Macchia, A. et al. Left ventricular systolic dysfunction, total mortality, and sudden death in patients with myocardial infarction treated with n-3 polyunsaturated fatty acids. Eur J Heart Failure 7, 904-909 (2005).
  31. Kumar, K.V. & Das, U.N. Effect of cis-unsaturated fatty acids, prostaglandins, and free radicals on angiotensin-converting enzyme activity in vitro. Proc Soc Exp Biol Med 214, 374-379 (1997).
  32. Das, U.N. Essential fatty acids and their metabolites could function as endogenous HMG-CoA reductase and ACE enzyme inhibitors, anti-arrhythmic, anti-hypertensive, anti-atherosclerotic, anti-inflammatory, cytoprotective, and cardioprotective molecules. Lipids Health Dis 7, 37 (2008).

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BENEFITS OF TAKING CAVSOR FOR PATIENTS WITH CHRONIC FATIGUE SYNDROME

Chronic fatigue syndrome (CFS), also called myalgic encephalomyelitis (ME), is characterized by persistent exhaustion and most often occurs between the ages of 20–40, although children are sometimes also affected [1]. According to the estimate by the US Centers for Disease Control and Prevention, CFS/ME affects more than one million people in the US [2]. As the name of this condition suggests, the main symptom is fatigue, both physical and mental, which is not alleviated by resting or sleeping [1]. Whereas many healthy people would find moderate physical exercise invigorating, exercise exacerbates exhaustion in CFS patients and may cause extreme exhaustion that lasts more than 24h [1, 3]. Fatigue may be accompanied by any of a number of other symptoms, some of which appear to be directly linked to fatigue: inability to concentrate, poor memory, headaches, insomnia, whereas others are not directly related to fatigue: pain in muscles, joints, lymph nodes, or stomach, headaches, sore throat, lymph node enlargement in the neck or armpits [1, 3].

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BENEFITS OF TAKING CAVSOR FOR PATIENTS WITH CHRONIC FATIGUE SYNDROME

Chronic fatigue syndrome (CFS), also called myalgic encephalomyelitis (ME), is characterized by persistent exhaustion and most often occurs between the ages of 20–40, although children are sometimes also affected [1]. According to the estimate by the US Centers for Disease Control and Prevention, CFS/ME affects more than one million people in the US [2]. As the name of this condition suggests, the main symptom is fatigue, both physical and mental, which is not alleviated by resting or sleeping [1]. Whereas many healthy people would find moderate physical exercise invigorating, exercise exacerbates exhaustion in CFS patients and may cause extreme exhaustion that lasts more than 24h [1, 3]. Fatigue may be accompanied by any of a number of other symptoms, some of which appear to be directly linked to fatigue: inability to concentrate, poor memory, headaches, insomnia, whereas others are not directly related to fatigue: pain in muscles, joints, lymph nodes, or stomach, headaches, sore throat, lymph node enlargement in the neck or armpits [1, 3].

 

The exact causes of CFS are unknown but may include infection (in particular, viral infection), immunity-related problems (in particular autoimmune responses), hormonal disturbances, or psychological stress [1, 3]. The results of studies of differential gene expression in CFS patients in comparison with healthy subjects, which were aimed at both elucidating the cause(s) of CFS and developing tools to reliably diagnose it, indicate that etiology of this disorder may be heterogeneous. For example, the study by Kaushik and colleagues [4] suggested a link to organophosphate compound exposure and virus infection, whereas that by Aspler and colleagues [5] implicated persistent inflammation. A later study by Frampton and colleagues [6] found that even using as many as 44 differentially expressed genes allowed to correctly diagnose only about two-thirds of CFS patients, suggesting a high degree of heterogeneity among them. Since the etiology of CFS is not firmly established, no definite cure exists, although most patients improve with time. As CFS is an “under investigated” disease, the US National Institutes of Health (NIH) has recently decided to strengthen its efforts to advance research on CFS and will investigate those symptoms developing soon after onset [2].

 

In the absence of a definite cure, there are indications that patients with CFS and related conditions have reduced levels of polyunsaturated fatty acids (PUFAs) and that PUFA supplementation may alleviate the CFS symptoms. A double-blind, placebo-controlled study conducted in the UK more than 25 years ago enrolled 63 patients with “postviral fatigue syndrome” who had the condition for one to three years (at that time, the criteria for CFS/ME diagnosis had not yet been defined, and these patients would likely have be diagnosed with CFS/ME today) and 32 healthy volunteers [7]. The authors found reduced levels of n-6 PUFAs in the erythrocyte membranes of fatigue syndrome patients in comparison with healthy controls. They conducted a three-month trial, in which some patients and healthy volunteers were given a supplement (8 × 500 mg daily) containing n-3 PUFAs (eicosapentaenoic [EPA] and docosahexaenoic [DHA] acids) and n-6 PUFAs (linoleic and γ-linolenic acids) and the patients were assessed at the first and the third months. In the fatigue syndrome group, the authors found an increase in PUFA levels and improvements over the baseline in 74% of the patients after one month and in 85% after three months, whereas improvements were found only in 17% and 23% of participants in the placebo group, respectively [7]; no adverse effects were noted.

 

In a separate publication, one of the co-authors of this study hypothesized that the beneficial effects of PUFA supplementation were likely due to the ability of viruses to suppress n-6 PUFA synthesis in the cells and the necessity of n-6 PUFAs for the antiviral effects of interferon [8].

 

A later small-scale study (22 CFS patients, 12 healthy subjects) by Maes and coworkers [9] conducted in Belgium found that the n-3/n-6 PUFA ratios were significantly lower in CFS patients than in normal subjects and were significantly correlated with CFS severity, thus lending support for the positive role n-3 rather than n-6 PUFAs in respect to CFS.

 

At least two hypotheses have been put forward to explain the mechanism of PUFA action in CFS. In a series of publications following their pilot study, Maes and colleagues suggested that treatment with n-3 PUFAs such as EPA and DHA would be beneficial for patients with CFS (both EPA and DHA are among the components of Cavsor). This and some other groups have also found reduced levels of n-3 PUFAs in patients with major depressive disorder (see references in [10]). It has been postulated that there is a link between depression and CFS, that both conditions are caused by “the aberrations in inflammatory, oxidative and nitrosative pathways” and that the beneficial effects of n-3 PUFAs are due to their well-known anti-inflammatory effects [10]. The anti-inflammatory action of n-3 PUFAs is well established and is thought to be due to several factors: (i) incorporation of n-3 PUFAs into the membranes of inflammatory cells at the expense of arachidonic acid, which is a precursor of pro-inflammatory eicosanoids; this reduces production of these inflammatory mediators; (ii) the n-3 PUFAs eicosapentaenoic acid and docosahexaenoic acid serve as precursors of anti-inflammatory mediators resolvins; and (iii) n-3 PUFAs modulate the expression of the genes encoding pro-inflammatory cytokines [11].

 

As mentioned above, infections, including viral ones, are thought to be one of the major factors that trigger CFS, and in its new research initiative on CFS the NIH is going to concentrate efforts on this cause [2]. Puri [12] has proposed a hypothesis to explain the likely link between persistent viral infections, n-3 PUFAs, and CFS. This hypothesis is based on the fact that the enzyme δ-6-desaturase, which is necessary for the biosynthesis of long-chain PUFAs (both n-3 and n-6), is inhibited by many viruses, resulting in PUFA deficit and consequently in multiple adverse effects, some of which are due to altered composition of cell membrane and some to changes in the PUFA-dependent synthesis of anti- and pro-inflammatory mediators.

 

The hypotheses put forward by Maes and coworkers and by Puri still need to be tested and large-scale trials are needed to elucidate the effects of PUFAs in CFS patients, along with a better understanding of the etiology of this disorder. Nevertheless, taking into account preliminary evidence described above, as well as various beneficial health effects of PUFA supplementation [13], it would make sense for CFS patients to consider taking PUFA supplements such as Cavsor.

 

References

  1. National Health Service, U.K. Chronic fatigue syndrome. http://www.nhs.uk/conditions/chronic-fatigue-syndrome/Pages/Introduction.aspx (2015).
  2. Cohen, J. NIH refocuses research into chronic fatigue syndrome. Science (2015).
  3. Mayo Clinic. Chronic fatigue syndrome. http://www.mayoclinic.org/diseases-conditions/chronic-fatigue-syndrome/basics/symptoms/con-20022009 (2016).
  4. Kaushik, N. et al. Gene expression in peripheral blood mononuclear cells from patients with chronic fatigue syndrome. J Clin Pathol 58, 826-832 (2005).
  5. Aspler, A.L., Bolshin, C., Vernon, S.D. & Broderick, G. Evidence of inflammatory immune signaling in chronic fatigue syndrome: A pilot study of gene expression in peripheral blood. Behav Brain Functions 4, 44 (2008).
  6. Frampton, D., Kerr, J., Harrison, T.J. & Kellam, P. Assessment of a 44 gene classifier for the evaluation of chronic fatigue syndrome from peripheral blood mononuclear cell gene expression. PLoS One 6, e16872 (2011).
  7. Behan, P.O., Behan, W.M. & Horrobin, D. Effect of high doses of essential fatty acids on the postviral fatigue syndrome. Acta Neurol Scand 82, 209-216 (1990).
  8. Horrobin, D.F. Post-viral fatigue syndrome, viral infections in atopic eczema, and essential fatty acids. Med Hypoth 32, 211-217 (1990).
  9. Maes, M., Mihaylova, I. & Leunis, J.C. In chronic fatigue syndrome, the decreased levels of omega-3 poly-unsaturated fatty acids are related to lowered serum zinc and defects in T cell activation. Neuroendocrinol Lett 26, 745-751 (2005).
  10. Maes, M. An intriguing and hitherto unexplained co-occurrence: Depression and chronic fatigue syndrome are manifestations of shared inflammatory, oxidative and nitrosative (IO&NS) pathways. Progr Neuro-psychopharmacol Biol Psychiatry 35, 784-794 (2011).
  11. Calder, P.C. n-3 polyunsaturated fatty acids, inflammation, and inflammatory diseases. Am J Clin Nutr 83, 1505S-1519S (2006).
  12. Puri, B.K. Long-chain polyunsaturated fatty acids and the pathophysiology of myalgic encephalomyelitis (chronic fatigue syndrome). J Clin Pathol 60, 122-124 (2007).
  13. Food and Agriculture Organization of the United Nations. Fats and fatty acids in human nutrition. http://www.fao.org/3/a-i1953e.pdf (2008).

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