Arterial Disease

Arterial disease accounts for the vast majority of patients that suffer from cardiovascular disease, and may be accompanied by diseases of the veins and heart. The primary arterial disease is atherosclerosis, a progressive disease of large and medium large arteries that is marked by the formation of plaques or atherosclerotic lesions in the endothelium. The term arteriosclerosis is the same pathology, and is used when discussing the atherosclerotic lesions that can occur in the smaller arterioles. The major complications of atherosclerosis include ischemic heart disease, myocardial infarction, and gangrene of the extremities. Atherosclerosis is the leading cause of death in North America, a percentage of the population that has been on the rise steadily since that turn of the last century.

Pathogenesis of atherosclerosis

Atherosclerotic plaques form in the tunica intima of elastic and muscular arteries as a result of the proliferation of intimal smooth muscle cells and the accumulation of fat. As the lesion develops smooth muscle cells release cytokines that stimulates the accumulation of mononuclear phagocytes, lymphocytes and neutrophils in the tunica intima. As the lesion progresses the endothelium ruptures and platelets begin to adhere to it. Eventually small capillaries penetrate the vessel wall and supply blood to the plaque, almost like a kind of malignant tumor. (Rubin and Farber 1990, 355-369)

There are a variety of hypotheses that describe the process of atherosclerotic plaquing. While there is good post-mortem evidence of what components comprises a plaque, and now better data on the risk factors for developing atherosclerosis, the actual mechanisms of how the plaque is formed is severely limited by our inability to actually observe this process in vivo. As a result there are several different theories that describe the mechanism of plaquing. Some of these theories are complimentary and some are antagonistic to each other. The most commonly held belief among medical doctors is the insudation hypothesis, which states that the lipid found in plaques is derived from plasma lipoproteins, specifically low density lipoproteins (LDL). This theory states that the atherosclerotic lesion begins with a mutation of a smooth muscle cell, perhaps from exposure to chemical or viral mutagens, resulting in focal regions of accumulation. Macrophages then scavenge LDL in the blood and transport the lipid directly into the tunica intima of the blood vessel. For some unexplainable reason there is additional damage to the lesion, exposing circulating platelets to subendothelial collagen, which promotes the release of growth factors by the platelets, as well as by local macrophages, that stimulate the proliferation of smooth muscle cells and make the lesion larger. There is the continued insudation of fat into the lesion by macrophages that then undergo degeneration. Eventually the surface of the plaque begins to ulcerate and a thrombus forms on the injured luminal surface. (Rubin and Farber 1990, 355-369)

The initial lesions found in atherosclerosis are thought to be fatty streaks, flat or slightly elevated lesions that contain lipid. Histologically, these streaks are comprised of lipid containing macrophages referred to as foam cells. While these fatty streaks can be found in both young children and the aged, the distribution of these streaks does not correspond with atherosclerotic lesions in adults. Another candidate for the initial lesion of atherosclerosis are intimal cells masses , which are white thickened areas at branch points in the aterial tree, containing smooth muscle cells but no lipid. (Rubin and Farber 1990, 355-369)

Whatever the initial lesion, the characteristic lesion of atherosclerosis is a fibro-fatty plaque consisting of a fibrous cap and an atheroma. The fibrous cap is a layer of thickened connective tissue containing fat-filled macrophages and smooth muscle cells. The atheroma is a necrotic mass of lipid that forms the middle portion of the lesion. Other components in the lesion of atherosclerosis include other blood-borne cells including lymphocytes. The complicated plaque of atherosclerosis is the clinically significant end-point for the formation of a plaque, characterized by:

1. Thrombosis: the aggregation of platelets, fibrin, clotting factors and blood-borne elements on and within the plaque
2. Neovascularization: of the cap and edges of lesion
3. Thinning: of the underlying tunica media
4. Calcification:within the atheroma and fibrous cap
5. Ulceration:of the fibrous cap. (Rubin and Farber 1990, 355-369)

The net result of these changes is the occlusion of the blood vessel and the formation of emboli, both of which end up producing ischemia in the tissues supplied by the atherosclerotic or otherwise occluded blood vessel.

It is thought that the process of atherosclerosis begins early in life, with the formation of intimal cell masses and fatty streaks. Regardless, the characteristic lesion of atherosclerosis requires as long as 20-30 years to form, and the clinically important complicated plaques only after several more decades of progressive development. In this respect atherosclerosis is primarily a disease of older adults. (Rubin and Farber 1990, 355-369)

Etiology of atherosclerosis

The causes of atherosclerosis are still not completely understood, with many convoluted and complicated mechanisms described. In this paper I will examine the most commonly held beliefs among the medical profession, as well an alternative to this perspective.

Medicine has defined several risk factors for the development of atherosclerosis, some of which may or may not prove to be entirely true. Many of these risk factors are based on a statistical analysis of the data called epidemiology, a process that helps to inform researchers of associations between certain factors and the incidence of disease. Although this process may identify groups in a population that may be vulnerable to a particular disease, it cannot indicate if a particular person will get a particular disease, and thus cannot take the place of an accurate, individualized health assessment. Further, epidemiological analysis cannot be used to demonstrate a causal relationship between a particular factor and a particular disease, although such conclusions are often drawn, particularly by the media and public health policy. For example, ‘red meat’ consumption is often associated with an increased risk of atherosclerosis, but epidemiological studies that find this association do not properly account for other variables in the diet. Unlike the First Nations peoples of the prairies that subsisted for millennia on the red meat of the buffalo, most North Americans eat ‘red meat’ sandwiched between two white buns slathered in condiments, accompanied by a side of fries and a large sugary soft-drink. And unlike the association found for modern North Americans, First Nations peoples that eat a traditional ‘red meat’ diet have a greatly reduced risk of atherosclerosis. Thus, when an association between something like ‘red meat’ consumption and atherosclerosis is found by epidemiological methods, it often reflects other issues or raises other questions, but it does not provide direct evidence of causation.

The vast majority of the approaches now utilized in the prevention and treatment of heart disease are based upon the Framingham Heart study, a cohort study of over 5000 adult men and women from the town of Framingham, Massachusetts. Begun in 1948, the participants of the study were analyzed for patterns related to the development of cardiovascular disease (CVD). A second generation cohort study was begun in 1971, involving a similar number of participants comprised of the original participants’ adult children and their spouses. A third generation cohort study is now being implemented. Given the duration and number of participants involved in the study, the Framingham Heart Study has proved to be a rich source of data for all kinds of researchers, who use a number of different methods to analyze the data and identify risk factors for CVD, including high blood pressure, high blood cholesterol, smoking, obesity, diabetes, and physical inactivity. The Framingham study has also provided additional information on the effects of factors such as blood triglyceride and LDL/HDL cholesterol levels, age, gender, and psychosocial issues. The Framingham data, the analyses and the theories derived from it has played an important role in the development of the modern medical curriculum, and has been influential in establishing hypertension and elevated serum cholesterol as the most prominent risk factors for the development of CVD.

Hypertension is commonly observed in atherosclerosis, simply due to the increased pressure by which the heart has to pump blood through the narrowed and occluded atherosclerotic vessels. Hypertensive patients are at greater risk of myocardial infarction and stroke. There are several causes of hypertension, such as renal artery stenosis or hyperthyroidism and must be ruled out.Essential hypertension is a term that has been given to hypertension when the cause is unknown, or cannot be directly observed. Designating hypertension as a risk factor for atherosclerosis however appears to be irrational – it is far more logical to suggest that essential hypertension is a symptom of the progressive effects of arterial damage. Unfortunately what may seem to be a fairly simple argument has been for the most part ignored by the medical profession, many of whom still encourage hypertensive patients to use medications to lower blood pressure, even though these same medications have no impact upon morbidity and mortality in hypertensive patients, and may directly interfere with normal physiological processes (Port et al 2000).

Elevated blood cholesterol and triglycerides are stated as being directly correlated with the development of ischemic heart disease and atherosclerosis. The hypdophobic nature of lipids in the blood means that fats must be transported with protein carriers, including chylomicrons, very low density lipoproteins (VLDL), low density lipoproteins (LDL) and high density lipoproteins (HDL). Chylomicrons are formed by the intestinal villi, and are comprised of globules of triglycerides, phospholipids and cholesterol covered by a protein coating. Chylomicrons are absorbed by the lacteal of a villus, transporting fats through the lymphatic system where they enter into systemic circulation at the left subclavian vein. The triglyceride component of the chylomicron is cleaved by lipoprotein lipase in the blood, where it is taken up by adipose and muscle cells. This leaves a cholesterol-rich lipoprotein remnant that is then taken up by the liver and excreted back into the intestine as bile salts, or repacked with triglycerides into VLDL, where it then reenters into circulation. Once again VLDL is acted upon by lipoprotein lipase, removing triglycerides from VLDL, forming intermediate-density lipoproteins (IDL) that are eventually converted into cholesterol-rich LDL. LDL is then taken up and processed by a variety of cells, leading to the accumulation of cholesterol within these cells. Unlike VLDL and LDL, which functions to transport cholesterol to peripheral cells, high density lipoproteins (HDL) functions to scavenge cholesterol and return it to the liver for excretion. Thus elevated levels of serum VLDL and LDL have been associated with a greater risk of CVD because they deposit cholesterol into peripheral cells, which according to the insudation hypothesis is the primary cause of atherosclerosis, whereas HDL is correlated with a lower risk because it removes cholesterol from cells. (Rubin and Farber 1990, 355-369)

Despite the elegance of this hypothesis and the determination of what are thought of as useful serum markers (e.g. total cholesterol, VLDL,LDL, and HDL) for the risk of cardiovascular disease, a complete analysis of the data suggests that there are a number of problems with the idea that cholesterol is pathogenic in CVD. When it comes to the argument that dietary cholesterol promotes hypercholesterolemia, the Framingham study clearly shows that men who ate the most cholesterol had exactly the same levels of cholesterol in their blood as those who ate the least cholesterol. And while the Framingham study does show that the highest risk of CVD is associated with total elevated serum cholesterol (18% occurrence), those participants with low to normal levels of serum cholesterol continue to be at significant risk (10-12% occurrence). Furthermore, another more recent cohort study called the Honolulu Heart program that examined 3572 Japanese/American men (aged 71–93 years) found that low serum cholesterol levels in the elderly is an indicator of increased mortality (Schatz et al 2001). All of this becomes extremely confusing.

Much of the impetus behind the cholesterol hypothesis is based on animal experimentation, such as the landmark study published by David Kritchevsky in 1954, who described the effects of feeding cholesterol to rabbits causing the formation of atheromas (Kritchevsky et al 1954). In another study published the following year Kritchevsky published a paper that described the benefits of consuming polyunsaturated fatty acids for lowering cholesterol levels. Some researchers criticized Kritchevsky’s research – after all, rabbits are herbivores and don’t normally eat cholesterol, unlike humans, who are omnivores and have a long history of eating cholesterol and saturated fat. Kritchevsky’s research marks the beginning of a drawn out campaign to get North American consumers to substitute traditionally-consumed cholesterol-rich foods such as butter for low cholesterol innovations such as refined corn oil. This marketing campaign had already begun much earlier in the century, but with a highly selective presentation of the preliminary scientific evidence, the industry-funded American Heart Association began to encourage the North American public to substitute butter, lard, beef and eggs with corn oil, margarine, chicken and cold cereal (Enig and Fallon 2003). Unfortunately these changes have been marked by an increasing incidence of cardiovascular disease in North America, which from 1900 to the mid 1960’s increased by 300%, and is now the single leading cause of death (Bergner 1997, 202-03)

The reason for the exclusion of data such as these from conventional medical thinking on CVD risks is unknown, but when considered it radically alters the perception that cholesterol-rich foods are responsible for elevated serum cholesterol, or that elevated serum cholesterol is an important a risk factor CVD. Of particular concern is the relatively recent use of a new class of drugs called statins, derived from red rice yeast, which are used to interrupt the synthesis of cholesterol and reduce LDL/cholesterol levels in the blood. Unfortunately, while statins indeed have been shown to reduce the risk of cardiovascular disease in patients with a history of myocardial infarction, they have also been shown to have number of adverse effects that make them unsuitable for general prevention in patients presenting with dyslipidemia. Some researchers have stated that the benefit of statins has nothing to do with the benefits of lowering cholesterol, but of promoting the stabilization of the lesion.

Hyperglycemia and atherosclerosis

Prolonged exposure to hyperglycemia has also been recognized another factor in the pathogenesis of atherosclerosis. Hyperglycemia induces a large number of alterations at the cellular level of vascular tissue that potentially accelerate the atherosclerotic process. Animal and human studies have indicated three major mechanisms that encompass most of the pathological alterations observed in the atherosclerosis:

1. nonenzymatic glycosylation
2. oxidative stress
3. protein kinase C (PKC) activation (Aronson and Rayfield 2002)

One of the important mechanisms responsible for the accelerated atherosclerosis in diabetes is the nonenzymatic reaction between glucose and proteins or lipoproteins in arterial walls, collectively known as Maillard, or browning reation. Glucose forms reversible early glycosylation products with reactive amino groups of circulating or vessel wall proteins to form advanced glycosylation end products (AGEs). AGEs normally accumulate with normal aging and at an accelerated rate in diabetic patients. In situations in which the local redox potential has been shifted to favor oxidant stress, AGEs formation is increased substantially, and can accelerate the atherosclerotic process (Aronson and Rayfield 2002).

Oxidative stress is another commonly described pathogenic mechanism for atherosclerosis. Hyperglycemia can increase oxidative stress through several pathways promoting the intracellular production of reactive oxygen species (ROS). There is also evidence that hyperglycemia may compromise natural antioxidant defenses. Reduced glutathione as well as reduced vitamin E have been reported in diabetic patients. Plasma and tissue levels of vitamin C are 40–50% lower in diabetic patients compared with nondiabetic subjects (Aronson and Rayfield 2002).

High glucose concentrations have been shown to activate the protein kinase C, a family of at least 12 isoforms of serine and threonine kinases. In vascular smooth muscle cells, PKC activation has been shown to modulate growth rate, DNA synthesis, and growth factor receptor turnover. Hyperglycemia-induced PKC activation also results in increased platelet derived growth factor-beta receptor expression on smooth muscle cells and other vascular wall cells, and increases the expression of transforming growth factor-beta (TGF-beta), which is thought to lead to thickening of capillary basement membrane (Aronson and Rayfield 2002).

Medical treatment

At this time modern medicine has no specific treatment for atherosclerosis, but is focused on inhibiting or alleviating signs and symptoms, or providing treatments that change or modify the results of laboratory investigations.

Hypertension is perceived as being a risk factor for atherosclerosis, and is managed symptomatically through the use of antihypertensive agents including:
• diuretics:promoting diuresis, decreasing plasma volume and edema, thereby decreasing cardiac output and blood pressure. Major drugs include thiazides (e.g. hydrochlorothiazide, depletes potassium), loop diuretics (e.g. furosemide, ethancrynic acid; depletes potassium),and potassium-sparing diuretics (e.g. triamterene, amiloride)
• beta-1 adrenergic antagonists: selectively antagonizes beta-1 receptors, often used in conjunction with thiazides (e.g. atenolol, metoprolol, propranolol)
• calcium channel antagonists: inhibits calcium ions from entering slow channels or voltage-sensitive areas of vascular smooth muscle and myocardium during depolarization (e.g. diltiazem verapamil nifedipine)
• angiotensin-converting enzyme (ACE) inhibitors: act as competitive inhibitors of ACE,reducing angiotensin II levels, and thus decreasing aldosterone secretion (e.g. captopril, enalapril, lisinopril, ramipril)
• aldosterone antagonists: competes with aldosterone receptor sites, reducing blood pressure and sodium reabsorption (e.g. eplerenone)
• alpha-adrenergic agonists: stimulate presynaptic alpha-2 adrenergic receptors in the brain stem, reducing sympathetic nervous activity (e.g. methyldopa) (Berkow 1992)

Hyperlipidemia is generally perceived as a risk factor for atherosclerosis largely based upon the use of hypolipidemic agents that lower serum cholesterol, and an observed reduction in the risk of coronary heart disease events and overall mortality. The primary hypolipidemic therapy consists of HMG-CoA reductase inhibitors or “statins” which inhibit the rate-limiting step of cholesterol synthesis in the liver, thereby lowering serum cholesterol, LDL-cholesterol, and triglyceride levels. Adverse effects include CoQ10 depletion (1), hepatotoxicity and myopathy. Example HMG-CoA reductase inhibitors include pravastatin, simvastatin, lovastatin, atorvastatin, and rosuvastatin.

On the preventative side, modern medicine typically recommends a series of general changes to diet and lifestyle to decrease the risk of CVD, based on the prevailing hypotheses, many of which continue to revolve around the insudation hypothesis. The American Heart Association has recently developed an “Eating Plan for Healthy Americans,” and is comprised of the following:

• Emphasis upon a variety of fruits and vegetables, eating five or more servings per day.
• Emphasis upon a variety of grain products, including whole grains, eating more than six or more servings per day.
• Emphasis upon fat-free and low-fat milk products, fish, legumes (beans), skinless poultry and lean meats.
• Emphasis upon fats and oils with 2 grams or less saturated fat per tablespoon, such as liquid and tub margarines, canola oil and olive oil.
• Limiting consumption of foods high in calories or low in nutrition, e.g. soft drinks and candy
• Limiting consumption of foods high in saturated fat, transfats and cholesterol, such as full-fat milk products, fatty meats, tropical oils, partially hydrogenated vegetable oils and egg yolks.
• Limiting consumption of sodium to less 2,400 milligrams per day.
• Limiting consumption of alcohol to no more than one alcoholic drink per day for women, and no more than two for men. “One drink” means it has no more than 1/2 ounce of pure alcohol, e.g. 12 oz. of beer, 4 oz. of wine, 1-1/2 oz. of 80-proof spirits or 1 oz. of 100-proof spirits.

Holistic treatment

Generally speaking, the holistic perspective on the origin of atherosclerosis is related to an underlying metabolic dysfunction caused by alterations in diet and lifestyle. This idea is based on sound epidemiological and anthropological research that indicates that the incidence of atherosclerosis is for the most part a disease of people that eat a highly refined modern diet, rich in carbohydrates, plentiful in oxidizing and toxic compounds, and deficient in key nutrients including minerals, vitamins, essential fatty acids, and plant-based antioxidants. Concomitant factors include a sedentary lifestyle (which promotes insulin resistance) and environmental pollutants, e.g. cigarettes, air pollution etc., some of which are easier to control (i.e. smoking, exercise) than others (i.e. air pollution). The result this exposure to environmental toxins, a lack of exercise, and a dysfunctional eating pattern are metabolic problems such as chronic hyperglycemia, insulin resistance, hyperinsulinemia and dyslipidemia, free radical production, and impaired detoxification. Thus the focus in holistic treatment is to reduce the glycemic load of the diet, and supplement with key nutrients that may be deficient and can enhance antioxidant and detoxification pathways in the body.

While the atheroma is fingered as the causal agent of atherosclerosis, and indeed, defines the nature of the condition, a holistic perspective suggests that the atheroma develops as a transient response to endothelial injury, to inhibit further endothelial injury by promoting a local thickening of the endothelial wall: essentially, chewing gum stuck in a crack of a dam about to burst. The transient and reversible nature of the atheroma suggests that if correct measures are taken to eliminate endothelial injury the atheroma will eventually be replaced by normal endothelial tissue. If the factors that cause damage to the endothelium are chronic however, the temporary method the body uses to protect against further endothelial injury becomes a secondary source of injury, narrowing the lumen of the vessels, placing stress on the heart, and then eventually, occluding the vessel so as to promote ischemia. The process of atherosclerosis is thus dependent upon chronic, underlying factors that promote the continuance of the atheroma, in much the same way that a scab that is constantly picked will never heal, and will result in a much larger lesion than originally sustained.

From a traditional herbal perspective, atherosclerosis can be seen as a dysfunction of blood, specifically, in its constitution and its movement. The constitution of the blood is in large part a manifestation of digestive processes, and thus an assessment of digestion should be carefully undertaken. Specifically, it is the job of the liver build, replenish and filter the blood, and thus problems relating to the constitution of blood (e.g. blood viscosity, dyslipidemia etc.) demonstrates a need for upregulating liver function with the use of cholagogues, e.g. Barberry (Berberis vulgaris), Turmeric (Curcuma longa), Dandelion (Taraxacum officinale), Chai Hu (Buplerum falcatum), Celandine Poppy (Chelidonium majus). In Chinese and Ayurvedic terms an increase in blood viscosity or dyslipidemia relates to the accumulation of phlegm, and thus phlegm-reducing (i.e. kaphahara) remedies such as Guggulu (Commiphora wighiti), Ginger (Zingiber officinale), Cayenne (Capsicum frutescens), Rosemary (Rosmarinus officinalis), Prickly Ash (Zanthoxylum clavaherculis) and Garlic (Allium sativum) can be used in conjunction with cholagogue remedies.

Given the obstructive nature of atherosclerosis the movement of blood is an extremely important consideration, and the nature of the treatment can be implemented based on the presenting signs and symptoms. Generally speaking, it is always wise to include stimulants such as Ginger, Cayenne and Garlic in any therapy directed to atherosclerosis to enhance the processing of blood via the liver, and to dispel the archetypal accumulation of phlegm that underlies the obstructive nature of the atheroma. In many cases however the atherosclerotic patient will present with a substantial deficiency, qi deficiency in Chinese terms, or an increase in vata in Ayuervedic terms. Besides typical symptoms of cold hands and feet, there will be chronic fatigue, poor digestion, and weak pulse. Treatment is orientated to building up the vital essence and restoring the natural heat of the body with nutritive, blood-moving herbs such as Dong Quai (Angelica sinensis), Huang Qi (Astragalus membranaceus), Guggulu (Commiphora wighiti), Dan Shen (Salvia miltiorrhiza), Ashwagandha (Withania somnifera), Ren Shen (Panax ginseng), Bai Zhu (Atractylodes macrocephala), prepared Fu Zi (Aconitum carmicheli) and purified Ativisha (Aconitum heterophyllum).

Besides the condition and movement of the blood, attention must also be directed to the integrity of the vessel walls. In Chinese medicine the vessels are said to be regulated by the Spleen, and thus in chronic Spleen qi deficiency the vessels are weak and become susceptible to damage and rupture. Once again, qi-restorative herbs such as those described above are similarly appropriate. Attention should also be directed to using botanicals that have a trophorestorative function on the endothelium. Many of these botanicals are particularly rich in polyphenols such as flavonoids and tannins (e.g. ellagitannins, proanthocyanidins) including Gingko (Ginkgo biloba), Bilberry (Vaccinium myrtillus), Arjuna (Terminalia arjuna), Amalaki (Phyllanthus emblica), Turmeric (Curcuma longa), Gotu Kola (Centella asiatica), Yarrow (Achillea millefolium) and Grape (Vitis vinifera) seed.

Overall, the holistic approach in the treatment of atherosclerosis is as follows:

1. Reduce the glycemic load of the diet. Adopt a low-carbohydrate diet, and eliminate all refined carbohydrates including sugar, candy, soda pop, cookies and deserts for a minimum period of two to three months. After which time, whole-grain carbohydrates can be rotated back into the diet.

2. Eliminate toxic foods from the diet. Including hydrogenated and trans-fats (e.g. margarine, deep-fried foods), feed-lot meat and farmed salmon, dairy.

3. Supplement for deficient nutrients.

• vitamin B complex, 100 mg daily
• folic acid, 1 g daily
• cobalamin, 1000 mcg daily
• vitamin C, 1-5 g bid-tid, to bowel tolerance
• vitamin E (d-alpha tocopherol), 400-800 IU daily, increase dose gradually
• EPA/DHA, 1000 mg each daily
• magnesium, 800 mg daily, in divided doses, with meals
• chromium,200-300 mcg daily, in divided doses, with meals
• selenium,100 mcg daily
• chelated multimineral, taken with the above minerals; or high quality kelp(seaweed) supplement (5-15 g daily)
• CoQ10,50 mg daily
• Flavonoids (mixed, e.g. quercitin, rutin, anthocyanidins), 3-5 g daily

4. Support liver, enhance detoxification: Barberry (Berberis vulgaris), Turmeric (Curcuma longa), Dandelion (Taraxacum officinale), Chai Hu (Buplerum falcatum), Celandine Poppy (Chelidonium majus) etc.

5. Promote circulation and blood flow, reduce blood viscosity (i.e. phlegm, kapha): Guggulu (Commiphora wighiti), Ginger (Zingiber officinale), Cayenne (Capsicum frutescens), Rosemary (Rosmarinus officinalis), Prickly Ash (Zanthoxylum clavaherculis), Garlic (Allium sativum), Pippali (Piper longum) etc.

6. Cardiovascular trophorestoration: Hawthorn (Crataegus spp.), Bilberry (Vaccinium myrtillus), Arjuna (Terminalia arjuna), Amalaki (Phyllanthus emblica), Turmeric (Curcuma longa), Gotu Kola (Centella asiatica), (Achillea millefolia) etc.

7. Rebuild the vital essence (i.e. qi, ojas): e.g. Dan Gui (Angelica sinensis), Huang Qi (Astragalus membranaceus), Guggulu (Commiphora wighiti), Dan Shen (Salvia miltiorrhiza), Ashwagandha (Withania somnifera), Ginseng (Panax ginseng), Bai Zhu (Atractylodes macrocephala) etc.

8. Exercise: in particular, anaerobic exercise (muscle-building) is more effective than aerobic exercise (jumping, running) to reduce insulin resistance, e.g. calisthenics (e.g. pushups, lunges, chin ups etc.), walking or bicycling uphill, hiking martial arts, weight-lifting; note that any exercise regimen should be implemented gradually