Conditions
Chronic Inflammation
Chronic inflammation can be triggered by cellular stress and dysfunction, such as that caused by excessive calorie consumption, elevated blood sugar levels, and oxidative stress.
Of the ten leading causes of mortality in the United States, chronic, low-level inflammation contributes to the pathogenesis of at least seven. These include heart disease, cancer, chronic lower respiratory disease, stroke, Alzheimer’s disease, diabetes, and nephritis. Inflammation has classically been viewed as an acute (short term) response to tissue injury that produces characteristic symptoms and usually resolves spontaneously. More contemporary revelations show chronic inflammation to be a major factor in the development of degenerative disease and loss of youthful functions.
Chronic inflammation can be triggered by cellular stress and dysfunction, such as that caused by excessive calorie consumption, elevated blood sugar levels, and oxidative stress. It is now clear that the destructive capacity of chronic inflammation is unprecedented among physiologic processes The danger of chronic, low-level inflammation is that its silent nature belies its destructive power.
In fact, stress-induced inflammation, once triggered, can persist undetected for years, or even decades, propagating cell death throughout the body. Due to the fact that it contributes so greatly to deterioration associated with the ageing process, this silent state of chronic inflammation has been coined “inflammation”.
Chronic low-level inflammation may be threatening your health at this very moment, without you realising it. On this page, you will learn about low-cost blood tests that can assess the inflammatory state within your body. You’ll also discover novel approaches that combat chronic inflammation to help avoid age-related health decline.
Cardiovascular diseases (CVD): Inflammation is an integral part of atherosclerosis (recall that oxidised low-density lipoprotein cholesterol stimulates the inflammatory response). Circulating inflammatory cytokines are predictive of peripheral arterial disease, heart failure, atrial fibrillation, stroke, and coronary heart disease.
Cancer: It was the results of several studies that there are links between chronic low-level inflammation and many types of cancer, including lymphoma, prostate, ovarian, pancreatic, colorectal and lung cancers. There are several mechanisms by which inflammation may contribute to carcinogenesis, including alterations in gene expression, DNA mutation, epigenetic alterations, promotion of tumour vascularization, and the expression of pro-inflammatory cytokines that have roles in cancer cell proliferation.
Diabetes: The infiltration of macrophages into fat tissue and their subsequent release of pro-inflammatory cytokines into circulation occur at a greater rate in type II diabetics than in non-diabetics. Pro-inflammatory cytokines clearly decrease if a person is insulin sensitive.
Age-related macular degeneration (AMD): An evaluation of 11 population-based studies encompassing over 41,000 patients demonstrated a clear association between elevated serum CRP levels (> 3 mg/L) and the incidence of late onset AMD. The risk of AMD in these high-CRP patients was increased over 2-fold compared with patients with CRP levels < 1 mg /L.
Chronic kidney disease (CKD): The chronic, low-grade inflammation in CKD can lead to the retention of several pro-inflammatory molecules in the blood (including cytokines, AGEs, and homocysteine). The reduced excretion of pro-inflammatory factors by the diseased kidney can accelerate the progression of chronic inflammatory disturbances elsewhere in the body, such as the cardiovascular system.
Osteoporosis: Various inflammatory cytokines (TNF-α, IL-1β, IL-6) are involved in normal bone metabolism. Osteoclasts, the cells that break down (resorb) bone tissue, are a type of macrophage and can be stimulated by pro-inflammatory factors. Systemic elevations in pro-inflammatory cytokines push bone metabolism towards reabsorption and have been observed to induce bone loss in persons with the periodontal disease, pancreatitis, inflammatory bowel disease, and rheumatoid arthritis. An increase in the levels of inflammatory cytokines is also a mechanism by which menopause stimulates bone loss.
Depression: It has been found in various studies that there is a small, but significant association between elevated IL-6 and CRP in depressed patients. At this stage, it is unclear whether inflammation leads to stress or vice versa, and there is data supporting both hypotheses.
Cognitive decline: Several observational studies have linked chronic low-level inflammation in older adults to cognitive decline and dementia, these include vascular dementia and Alzheimer’s disease.
Others: Elevations in circulating inflammatory cytokines are associated with several other conditions, both inflammatory (rheumatoid arthritis, IBD/Crohn’s disease, pancreatitis) and non-inflammatory (anaemia, fibromyalgia, frailty, sarcopenia, cachexia, and muscle wasting). Again, whether inflammation incites these conditions or results from them is unclear and requires further investigation.
It has been found that inflammation, which is the adaptive immune response to tissue injury or infection, plays a central role in metabolism in a variety of organisms. At its most basic level, an acute inflammatory response is triggered by either tissue injury (such as trauma, exposure to heat or chemicals); or infection by viruses, bacteria, parasites, or fungi.
The classic manifestation of acute inflammation is characterised by four cardinal signs:
1) Redness and 2) heat result from the increased blood flow to the site of injury.
3) Swelling results from the accumulation of fluid at the injury site, a consequence of the increased blood flow.
4) Finally, swelling can compress nerve endings near the injury, causing the characteristic pain associated with inflammation. Pain is also important to make the organism aware of the tissue damage.
5) Additionally, inflammation in a joint usually results in impairment of function, which has the effect of limiting movement and forcing rest of the injured joint to aid in healing.
A well-controlled acute inflammatory response has several protective roles:
* It prevents the spread of infectious agents and damage to nearby tissues;
* helps to remove damaged tissue and pathogens, and;
*assists the body’s repair processes.
However, the third type of stimuli, cellular stress and malfunction, triggers chronic inflammation, which, rather than benefiting health, contributes to disease and age-related deterioration via numerous mechanisms.
Mitochondrial dysfunction arises consequent of exposure to exogenous (external environmental toxins, tobacco smoke) and endogenous (internal reactive oxygen species) stressors, and as a result of the ageing process itself. For example, a by-product of mitochondrial energy generation is the creation of free radical molecules. Free radicals can damage cellular structures and initiate a cascade of pro-inflammatory genetic signals that ultimately results in cell death (apoptosis), or worse, uncontrolled cell growth - the hallmark of cancer.
Circulating sugars, primarily glucose and fructose, are culprits as well. When these “blood sugars” come in contact with proteins and lipids a damaging reaction leads to the formation of compounds called advanced glycation end products (AGEs). AGEs bind to the cell-surface receptor called receptor for advanced glycation end products, or RAGE.
Uric acid (urate) crystals, which can be deposited in joints during gouty arthritis. If a patient has elevated levels it might be a risk factor for kidney disease, hypertension, and metabolic syndrome (Oxidised lipoproteins (such as LDL)), a significant contributor to atherosclerotic plaques
Homocysteine, a non-protein-forming amino acid that is a marker and risk factor for cardiovascular disease, and may increase bone fracture risk.
Together, these pro-inflammatory instigators promote a perpetual low-level chronic inflammatory state called para-inflammation. Although it progresses silently, para-inflammation presents a major threat to the health and longevity of all ageing humans. Chronic, low-level inflammation is associated with common diseases including cancer, type II diabetes, osteoporosis, cardiovascular diseases, and others. If it is possible for a patient to target the myriad of physiological variables that can inaugurate an inflammatory response, they can effectively temper chronic inflammation and reduce their risk for inflammatory diseases.
There are several risk factors which increase the likelihood of establishing and maintaining a low-level inflammatory response. These include:
Age: In contrast to younger individuals (whose levels of inflammatory cytokines typically increase only in response to infection or injury), older adults can have consistently elevated levels of several inflammatory molecules, especially IL-6 and TNF-α. These elevations are observed even in healthy older individuals. While the reasoning for this age-associated increase in inflammatory markers is not thoroughly understood, it may reflect cumulative mitochondrial dysfunction and oxidative damage or may be the result of other risk factors associated with age (such as increases in visceral body fat or reductions in sex hormones; see below).
Obesity: Fat tissue is an endocrine organ, which stores and secretes multiple hormones and cytokines into circulation and affecting metabolism throughout the body. Visceral fat cells can produce three times the amount of IL-6 as fats cells elsewhere in the body, and in overweight individuals, may be producing up to 35% of the total IL-6 in the body.
Diet: A diet high in saturated fat is associated with higher pro-inflammatory markers, particularly in diabetic or overweight individuals. The increases in markers of inflammation due to synthetic trans-fats may be more pronounced in individuals that are also overweight.
General dietary over-consumption is a major contributor to inflammation and other detrimental age-related processes in the modern world. Therefore, eating a calorie-restricted diet is an effective means of relieving physiologic stressors. Indeed, several studies show that calorie restriction provides powerful protection against inflammation.
Low sex hormones: Amongst their many roles in biology, sex hormones also modulate the immune/inflammatory response. The cells that mediate inflammation (such as neutrophils and macrophages) have receptors for oestrogens and androgens that enable them to selectively respond to sex hormone levels in many tissues.
Hormone replacement therapy (HRT) may partially exert its protective effects through an attenuation of the inflammatory response. Reductions in the risks of coronary heart disease and inflammatory bowel disease in some individuals, as well as levels of some circulating inflammatory cytokines (including IL-1B, IL-8, and TNF-α) has been observed in some studies of women on hormone replacement therapy.
Smoking: Cigarette smoke contains several inducers of inflammation, particularly reactive oxygen species. Chronic smoking increases production of several pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, IL-8), while simultaneously reducing production of anti-inflammatory molecules. Smoking also increases the risk of periodontal disease, an independent risk factor for increasing systemic inflammation.
Sleep Disorders: Production of inflammatory cytokines (TNF-α and IL-1β) appears to follow a circadian rhythm and may be involved in the regulation of sleep in animals and humans. Disruption of normal sleep can lead to daytime elevations of these pro-inflammatory molecules.
Periodontal disease can produce a systemic inflammatory response that may affect several other systems, such as the heart and kidneys. It is through this mechanism that periodontal disease is thought to be a risk factor for cardiovascular diseases (stimulated by the release of the stress hormone cortisol), both of which are independent causes of inflammation.
Excess Blood Glucose Fuels Inflammatory Fires
When glucose is properly utilised, our cells produce energy efficiently. As cellular sensitivity to insulin diminishes, excess glucose accumulates in our bloodstream. Like the spilled gasoline, excess blood glucose creates a highly combustible environment from which oxidative and inflammatory fires chronically erupt. Excess glucose not used for energy production converts to triglycerides that are either stored as unwanted body fat or accumulate in the blood where they contribute to the formation of atherosclerotic plaque.
As an ageing human, you face a daily onslaught of excess glucose that poses a grave risk to your health and longevity. Surplus glucose relentlessly reacts with your body’s proteins, causing damaging glycation reactions while fuelling the fires of chronic inflammation and inciting the production of destructive free radicals.
Avert Glycation and Inflammation by Controlling Glucose Levels with Green Coffee Bean Extract. Unroasted coffee beans, once purified and standardised, produce high levels of chlorogenic acid and other beneficial polyphenols that can suppress excess blood glucose levels. Human clinical trials support the role of chlorogenic acid-rich green coffee bean extract in promoting healthy blood sugar control and reducing disease risk.
Chronic inflammation or para-inflammation is generally not treated on its own by mainstream physicians. Interventions in conventional medicine are usually only undertaken when the inflammation occurs in association with another medical condition (such as arthritis). Currently, conventional preventive medical approaches to inflammation are limited to the use of CRP to predict cardiovascular disease in high-risk subjects, and the prophylactic use of drugs like aspirin to inhibit the inflammatory cascade linked to thrombosis (uncontrolled blood clotting). Indeed, the potentially asymptomatic nature of low-grade inflammation is such that elevations of pro-inflammatory cytokines may progress undetected for some time, only being discovered after they have had time to cause enough cellular damage to produce disease symptoms. As future studies solidify the association between inflammatory mediators and different diseases, early detection of cytokine aberrations and anti-inflammatory therapy to reduce disease risk may gain more mainstream acceptance.
Your Doctor at Health Renewal will manage chronic inflammation through a consultation and thorough examination. You may be requested to undergo blood tests.
The initial medical consultation at Health Renewal will be approximately 45 minutes. You will have to complete an in-depth questionnaire before the consultation so please arrive 20 minutes prior to your appointment. During the 45 minute consultation, your Health Renewal doctor will obtain a full medical history from you to determine your personal risk. A physical examination will be done after which he/she will decide which blood tests need to be requested from your local pathology laboratory. These results will then be analysed by your Doctor and this will be discussed with you at your follow-up appointments. This will determine whether a definite deficiency exists and you will be advised on your treatment options. These options may range from prescription medications, nutraceuticals, bio-identical hormonal creams or tablets or alternatively to having bio-identical implants or pellets inserted superficially under the skin.
Inflammation itself is not a disease, but is featured, to varying degrees, in adverse health conditions. What follows is a summary of dietary and supplemental approaches to addressing general chronic inflammation and para-inflammation. As many types of general inflammation often occur without additional symptoms, most of the strategies listed below are based on their ability to reduce circulating inflammatory cytokines, the hallmark of the para-inflammatory state
Macronutrients and Energy Balance.
Macronutrient content (particularly the types and levels of carbohydrates and fats) can have a significant effect on the progression of inflammation (as measured by increases in pro-inflammatory markers). Diets with relatively high glycemic index (GI) and glycemic load (GL) have been associated with elevated risk of coronary heart disease, stroke, and type 2 diabetes mellitus, particularly among overweight individuals, and have been associated with modest increases in pro-inflammatory markers in multiple studies. As discussed previously, some dietary fats (particularly saturated and synthetic trans- fats) increase inflammation occurrence, while omega-3 polyunsaturated fats appear to be anti-inflammatory. Since fat tissue (especially abdominal fat) expresses inflammatory cytokines, obesity can be a major cause of low-grade, systemic inflammation. Thus, it is important that total energy intake is proportional to energy expenditure, to avoid the deposition of abdominal fat. Obesity-induced increases in inflammatory cytokines appear to be reversible with fat loss. In a dramatic example, weight loss in a group of 20 severely obese individuals reduced IL-6 by 22% and CRP by almost 50%.
Amongst the most anti-inflammatory nutrients (based on the model and study data) are magnesium, beta-carotene, turmeric (curcumin), genistein, and tea. The most pro-inflammatory included carbohydrates, total- and saturated fat, and cholesterol. The index may provide a useful metric for accessing the overall inflammatory potential of an individual diet.
Exercise. Energy expenditure through exercise lowers multiple cytokines and pro-inflammatory molecules independently of weight loss. While muscle contraction initially results in a pro-inflammatory state, it paradoxically lowers systemic inflammation.
Fiber. In an analysis of 7 studies on the relationship between weight loss and hs-CRP, increased fibre consumption correlated with significantly greater reductions in hs-CRP concentrations.
Micronutrients
Magnesium. There is a significant association between greater dietary magnesium and the lower levels of the inflammation-associated proteins homocysteine and fibrinogen. Magnesium was rated as the most anti-inflammatory dietary factor in the Dietary Inflammatory index, which rated 42 common dietary constituents on their ability to reduce CRP levels based on human and animal experimental and observation data.
Vitamin D. Vitamin D appears to exert anti-inflammatory activity by the suppression of pro-inflammatory prostaglandins, and inhibition of the inflammatory mediator NF-κβ. Vitamin D deficiencies are more common amongst patients with inflammatory diseases (including rheumatoid arthritis, inflammatory bowel disease, systemic lupus erythematosus, and diabetes) than in healthy individuals. They also occur more frequently in populations that are prone to low-level inflammation, such as obese individuals and the elderly.
Vitamin E. Vitamin E functions as an antioxidant in the body. Specifically, vitamin E is incorporated into low-density lipoprotein (LDL) particles and protects them against oxidative damage; it seems to guard against atherosclerosis via other mechanisms as well. The gamma-tocopherol form of vitamin E appears to complement the anti-inflammatory action of alpha-tocopherol. The combination of alpha-tocopherol and gamma-tocopherol supplementation appears to be superior to either supplementation alone on biomarkers of oxidative stress and inflammation.
Other Dietary Factors
Resveratrol and Pterostilbene. The exact mechanism by which resveratrol exerts anti-inflammatory activity has not been established, although it inhibits a variety of pro-inflammatory compounds (cyclooxygenase, TNF-α, IL-1β, IL-6, NF-κβ) in animal models and human cell culture. Resveratrol may be protective against general, low-level para-inflammation as well: when taken with a single high-fat, high-carbohydrate meal (930 kcal), resveratrol (100 mg) prevented the sharp post-meal increases in markers of oxidation and inflammation in a small crossover study of 10 healthy volunteers.
Curcumin. Extensive in vitro and animal studies have examined the effects of curcumin on experimentally-induced inflammatory diseases (atherosclerosis, arthritis, diabetes, liver disease, gastrointestinal disorders, and cancers) and disease markers (lipoxygenase, cyclooxygenase, TNF-α, IL-1β, NF-κβ, and others). Most of the small randomised controlled trials of curcumin have consistently shown patient improvements in several inflammatory diseases, including psoriasis, irritable bowel syndrome, rheumatoid arthritis, and inflammatory eye disease.
Tea polyphenols. The anti-inflammatory effects of green and black tea polyphenols have been substantiated by dozens of in vitro and animal studies. In clinical interventions, black tea appears to be more successful in reducing inflammatory markers than green tea. A 25% reduction in CRP was also observed in a small trial of healthy, non-smoking men consuming a black tea extract (equivalent to 4 cups of tea/day) for 6 weeks. A similar average reduction was observed in a larger study of healthy, individuals at high risk for coronary heart disease, but revealed a more dramatic 40-50% reduction in CRP amongst individuals with the highest starting CRP values (>3 mg/L).
Carotenoids. In the Women’s Health and Aging Study, participants with the highest blood levels of α-carotene and total carotenoids were significantly more likely to have the lower IL-6 levels than participants with low carotenoid levels at the onset of the study. Participants with the lowest blood levels of α- and β-carotene, lutein/zeaxanthin, or total carotenoids were more likely to experience increases in IL-6 over a period of 2 years.
DHEA. Low levels of sex hormones are associated with systemic increases in inflammatory markers; DHEA (dehydroepiandrosterone) is an adrenal steroid hormone, the precursor to the sex steroids testosterone and oestrogen. DHEA is abundant in youth, but steady declines with advancing age and may be partially responsible for age-related decreases sex steroids. In cell culture and animal models, DHEA can suppress inflammatory cytokine activity, in some cases more effectively than either testosterone or oestrogen. Chronic inflammation may itself reduce DHEA levels. DHEA supplementation in elderly volunteers (50 mg/day for 2 years) significantly decreased TNF-α and IL-6 levels, as well as lowered visceral fat mass and improved glucose tolerance (both associated with inflammation).
Fish Oil. This is the best source of the omega-3 fatty acids eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) that can only be synthesised to a limited extent in humans, which is why fish oil supplementation is so critical. Omega-3 fatty acids have been well studied for their prevention of cardiovascular disease and mortality in tens of thousands of patients; the anti-inflammatory effects of omega-3’s contribute to this activity. It has also been successfully proven to improving patient outcomes in scores of studies of other inflammatory diseases, particularly asthma, inflammatory bowel disease, and rheumatoid arthritis.
The association between greater fish oil/omega-3 consumption and reduced systemic inflammation is substantiated by data from several large observational trials. In 855 healthy participants from the Health Professionals Follow-Up Study, intake of omega-3 fatty acids was associated with lower plasma levels of markers of TNF-α activity; interestingly, high intake of both omega-3 and omega-6 fatty acids (which are usually assumed to be pro-inflammatory) was associated with the lowest level of inflammation. The Nurses’ Health Study I cohort of 727 women revealed lower concentrations of inflammatory markers (including CRP and IL-6) amongst those in the top 20% of omega-3 consumption when compared to those who consumed the least amount. In the ATTICA study of over 3000 Greek men and women without any evidence of cardiovascular disease, participants who consumed over 300g of fish per week had, on average, 33% lower CRP, 33% lower IL-6, and 21% lower TNF-α than participants who did not consume fish. In a sample of 5,677 men and women without cardiovascular disease from the Multi-Ethnic Study of Atherosclerosis (MESA) cohort, long-chain omega-3 intake (from fish or supplements) was associated with reduced plasma concentrations of multiple inflammatory markers (including CRP, IL-6, and TNF-α receptor, a measure of TNF-α activity).
N-acetyl cysteine (NAC). Activation of the NF-κB pathway plays a central role in the activation of inflammatory cytokine genes; N-acetyl cysteine inhibits NF-κβ in cell culture, lowering expression of cytokines such as IL-6 and IL-8. Data establishing the effects of NAC on lowering chronic inflammation in humans is limited but shows promise. NAC supplementation for 8 weeks demonstrated the modest, but statistically significant decreases in circulating IL-6 levels in patients with chronic kidney disease. The effects were more pronounced in persons with significant inflammation at the start of the study (as measured by hs-CRP). NAC also reduced markers of systemic inflammation in a small study of patients with burn injuries.
Boswellia. Boswellia serrata (frankincense) is a traditional anti-arthritic in Ayurvedic medicine; its anti-inflammatory properties have been attributed to the specific inhibition of 5-LOX and reduction in the production of pro-inflammatory leukotrienes by boswelic acids, a constituent of the Boswellia gum resin.
Bromelain. The anti-inflammatory activity of the proteolytic enzyme preparation bromelain has been attributed to its ability to reduce COX-2 activity, decrease prostaglandin and thromboxane synthesis, lower circulating fibrinogen levels, and reduce cellular adhesion of pro-inflammatory white blood cells to the sites of inflammation. Another study comparing a standardised commercial enzyme preparation containing bromelain with diclofenac reached the same conclusion. The study reported that the supplement containing bromelain (90 mg, three times daily) to be as effective as diclofenac (50 mg, twice daily) in improving the symptoms of osteoarthritis of the knee. Patients reported comparable reductions in joint tenderness, pain and swelling, and improvement in range of motion at the end of the study. The investigators found bromelain to be as good as diclofenac on a standard pain assessment scale and to be better than the drug in reducing pain at rest.
Reactive oxygen species generated during mitochondrial respiration contribute to inflammation, as outlined above. Ageing individuals are especially susceptible to mitochondria-related oxidative stress since mitochondria become increasingly dysfunctional with age. Taking steps to support mitochondrial integrity and efficiency can help alleviate some of the systemic oxidative and inflammatory burden caused by poorly functioning mitochondria. Two nutrients, coenzyme Q10 (CoQ10) and the pyrrloquinoline quinone (PQQ) are powerful mitochondrial protectants, and studies support an anti-inflammatory role for these compounds.
Pyrroloquinoline quinone is a cofactor for enzymes critically important for cellular energy homeostases and redox balance. Several studies have shown that PQQ exerts a protective effective during circumstantial mitochondrial stress and increased the oxidative load. During periods of limited oxygen supply to the cardiac tissue, a dramatic spike in oxidative stress and subsequent inflammation damages cells; the findings from this animal model indicate that PQQ can stave off this inflammatory cell destruction by preserving mitochondrial efficiency in adverse conditions.
Coenzyme Q10 is an indispensable intermediary in mitochondrial ATP production. Studies have shown that CoQ10 levels are low during inflammatory conditions. In one investigation, patients with septic shock were found to have CoQ10 levels substantially lower than healthy individuals, and, among patients, lower CoQ10 levels correlated with higher levels of an inflammatory mediator called VCAM.
The role of elevated blood sugar and glycation end products in initiating an inflammatory storm has been discussed above. Fortunately, in addition to reducing caloric intake to suppress both fasting and post-meal glucose concentrations, some natural compounds ameliorate the glycation process and may help rein in the sugar-induced inflammatory cascade. Chief among these anti-glycation nutrients are benfotiamine, a member of the B-vitamin family, and carnosine, an amino acid.
Benfotiamine has been used to target diabetic complications since the mid of the 1990’s. More recent evidence continues to support its use as a powerful protector against blood sugar-induced tissue damage. Laboratory experiments have shown that, in addition to blocking glycation reactions, benfotiamine may regulate inflammation more directly by modulating COX and LOX enzyme activity.
Carnosine exerts a range of favourable biochemical effects within the body; it powerfully blunts glycation reactions and eases oxidative stress. In addition, several experiments have revealed a marked ability of carnosine to suppress inflammation in various cell types.
A multi-gene DNA test can routinely be added to assessment of
It includes analysis of variation in clinically useful genes that may contribute to abnormal cholesterol levels,
Some of these abnormalities contribute to the development of type II diabetes, obesity and hypertension. Oxidative stress, detoxification of carcinogens and oestrogen exposure are also important considerations in this context.
This pathology supported genetic test is performed in conjunction with assessment of any food allergy or intolerances known to be associated with many chronic disorders. The results of the genetic test are combined with clinical indicators and lifestyle factors to identify a combination of risk factors that may lead to disease development or the progression if left untreated.
For all health conditions, the nutraceuticals are individually tailored by the Health Renewal Doctor. The doctor will decide- based on your history, physical examination and blood tests what would be the best for you and your specific needs and/or deficiencies. It cannot be overemphasised that one must not self-medicate. Self-Medicating is done when a person takes prescription medication or nutraceuticals on their own without a doctor's supervision and/or consent. By not having a physical examination and blood testing done by a qualified and practising integrative medical practitioner, you could be not treating vital deficiencies or conditions such as elevated blood pressure, high sugar level, high stress levels (that can lead to adrenal burnout ) and high blood clotting factors that could lead to heart attacks and stroke. In addition, the aggressive program of dietary supplementation should not be launched without the supervision of a qualified physician. Several of the nutrients suggested in this protocol may have adverse effects. There is no single supplement prescribed to clients as there is no magic bullet that can support all the essential nutrients that one's body needs. Today's food is not functional and we need to supplement in order to maintain optimal bodily functions and nutrition.
Make an appointment to consult with your Health Renewal Doctor who is an integrative doctor and he or she will assist you in determining your risk factors and how best to prevent any problems or conditions that you may be susceptible to. The importance of early management of any condition cannot be overstated. Once certain conditions set in and damage to organs occurs, complete recovery may be difficult to attain. Best results for prevention and longevity is early detection of a possible problem combined with conventional treatments, nutritional supplements and a healthy diet and lifestyle.
The initial medical consultation at Health Renewal will be approximately 45 minutes. As this is a prolonged medical consultation, the initial consultation fee will be R 975 on arrival (for non-loyalty programme members) you will have to complete an in-depth questionnaire before the consultation so please arrive 20 minutes before the time. During the 45 minute consultation, your Health Renewal doctor will obtain a FULL medical history from you to determine your personal risk. A physical examination will be done after which the Doctor will decide which blood tests need to be requested from your local pathology laboratory. If you have a medical aid, these should be able to be claimed as well.
Once your blood results are received, they will then be analysed by your Health Renewal doctor who will begin working on a unique prescription plan for you with the compounding pharmacy. At your pre-scheduled second appointment 2 weeks later, the results and examination findings will be discussed with you. This will determine what abnormalities or deficiencies exist and you will be advised on your treatment options. These options may range from prescription medications, nutraceuticals, bio-identical hormonal creams or tablets or alternatively to having bio-identical implants or pellets inserted.
In office treatments such as carboxytherapy may also be recommended for certain conditions such as hair loss, erectile dysfunction ED, menopause or PMS. If you need to lose weight our Renewal Institute Diet may be recommended. All these recommendations will be summarised on a sheet or print out which you can take home with you. The nutraceuticals offered at Health Renewal are of superior quality (Solgar) and are not rancid nor contain Hg (mercury ) or PCB'S (which is very important for Omega 3 Essential fatty acids EFA's). They are also free of gluten, preservatives, wheat, dairy, soy, yeast, sugar, artificial flavour, sweetener and colour. We have a great professional team made up of doctors, trained and registered nurses and therapists to support you at any time.
1. You are kindly requested to bring any supplements that you are currently taking, along to your consultation. The doctor can check the ingredients in this and take it into account when prescribing a treatment plan for you.
2. Also, if you have had any blood work done in the past 6 months, please bring the results along to the consultation. Should you not be in possession of the hard copies, please request these results from the lab you visited. Usually, your ID number is sufficient.
Depending on the exact prescription given, you may be required to return to the doctor within 1-4 months’ time, in order to ensure optimum hormone levels are achieved. This will be determined by a repeat blood test and may be requested by your Health Renewal doctor.
You should ensure that you are current with your gynaecological visits/breast exams/mammograms (for female patients) and prostate exams (for male patients) as recommended by your GP/gynaecologist.
Depending on which form of supplementation you and your Health Renewal Doctor have decided on, one could expect to follow up with your physician from anything between every 3 months to once every 6 months.
General Support
Magnesium: 100 – 800 elemental milligrams of highly-absorbable magnesium
Vitamin D: 5000 – 8000 IU daily (depending on blood test results; optimal blood levels are between 50 and 80 ng/mL)
Vitamin A: 500 IU acetate and 4500 IU beta-carotene daily
Natural Vitamin E: 100 – 400 IU alpha-tocopherol and 200 mg gamma-tocopherol daily
Fish oil (with olive polyphenols and sesame lignans): providing 1400 mg EPA and 1000 mg DHA daily
Zinc: 30 mg daily
Selenium: 200 mcg daily
DHEA: 15 – 25 mg daily for women, and 25 – 75 mg daily for men (depending on blood test results)
Antioxidants
Trans-resveratrol: 100 – 500 mg daily
Trans-pterostilbene: 0.5 – 50 mg daily
Green tea extract, standardized to 98% polyphenols: 725 – 1450 mg daily
Black tea extract, standardized to 25% theaflavins: 350 mg daily
N-Acetylcysteine: 600 – 1200 mg daily
Mechanism-Specific Support
Curcumin (as highly absorbed BCM-95®): 400 – 800 mg daily
Boswellia serrata extract (as highly absorbed AprèsFlex™), standardized to 20% AKBA: 100 mg daily
Bromelain (enteric coated): 500 – 1000 mg daily
Optimizing Glucose Levels and Targeting Advanced Glycation End Products
Green coffee bean extract, standardized to 50% chlorogenic acid: 200 – 400 mg before each meal, up to three times daily
Benfotiamine: 150 – 1000 mg daily
L-carnosine: 500 – 1500 mg daily
Supporting Mitochondrial Function
Pyrroloquinoline quinone: 10 – 20 mg daily
CoQ10 (as ubiquinol): 100 – 200 mg daily
The importance of early management of any condition cannot be overstated. Once certain conditions set in and damage to organs occurs, complete recovery may be difficult to attain. Best results for prevention and longevity is early detection of a possible problem combined with conventional treatments, nutritional supplements and a healthy diet and lifestyle.
Here are ten quotes from great thinkers to challenge, motivate and inspire us to exercise, eat right and live healthier lives: Health and intellect are the two blessings of life.
Of the ten leading causes of mortality in the United States, chronic, low-level inflammation contributes to the pathogenesis of at least seven. These include heart disease, cancer, chronic lower respiratory disease, stroke, Alzheimer’s disease, diabetes, and nephritis. Inflammation has classically been viewed as an acute (short term) response to tissue injury that produces characteristic symptoms and usually resolves spontaneously. More contemporary revelations show chronic inflammation to be a major factor in the development of degenerative disease and loss of youthful functions.
Chronic inflammation can be triggered by cellular stress and dysfunction, such as that caused by excessive calorie consumption, elevated blood sugar levels, and oxidative stress. It is now clear that the destructive capacity of chronic inflammation is unprecedented among physiologic processes The danger of chronic, low-level inflammation is that its silent nature belies its destructive power.
In fact, stress-induced inflammation, once triggered, can persist undetected for years, or even decades, propagating cell death throughout the body. Due to the fact that it contributes so greatly to deterioration associated with the ageing process, this silent state of chronic inflammation has been coined “inflammation”.
Chronic low-level inflammation may be threatening your health at this very moment, without you realising it. On this page, you will learn about low-cost blood tests that can assess the inflammatory state within your body. You’ll also discover novel approaches that combat chronic inflammation to help avoid age-related health decline.
Cardiovascular diseases (CVD): Inflammation is an integral part of atherosclerosis (recall that oxidised low-density lipoprotein cholesterol stimulates the inflammatory response). Circulating inflammatory cytokines are predictive of peripheral arterial disease, heart failure, atrial fibrillation, stroke, and coronary heart disease.
Cancer: It was the results of several studies that there are links between chronic low-level inflammation and many types of cancer, including lymphoma, prostate, ovarian, pancreatic, colorectal and lung cancers. There are several mechanisms by which inflammation may contribute to carcinogenesis, including alterations in gene expression, DNA mutation, epigenetic alterations, promotion of tumour vascularization, and the expression of pro-inflammatory cytokines that have roles in cancer cell proliferation.
Diabetes: The infiltration of macrophages into fat tissue and their subsequent release of pro-inflammatory cytokines into circulation occur at a greater rate in type II diabetics than in non-diabetics. Pro-inflammatory cytokines clearly decrease if a person is insulin sensitive.
Age-related macular degeneration (AMD): An evaluation of 11 population-based studies encompassing over 41,000 patients demonstrated a clear association between elevated serum CRP levels (> 3 mg/L) and the incidence of late onset AMD. The risk of AMD in these high-CRP patients was increased over 2-fold compared with patients with CRP levels < 1 mg /L.
Chronic kidney disease (CKD): The chronic, low-grade inflammation in CKD can lead to the retention of several pro-inflammatory molecules in the blood (including cytokines, AGEs, and homocysteine). The reduced excretion of pro-inflammatory factors by the diseased kidney can accelerate the progression of chronic inflammatory disturbances elsewhere in the body, such as the cardiovascular system.
Osteoporosis: Various inflammatory cytokines (TNF-α, IL-1β, IL-6) are involved in normal bone metabolism. Osteoclasts, the cells that break down (resorb) bone tissue, are a type of macrophage and can be stimulated by pro-inflammatory factors. Systemic elevations in pro-inflammatory cytokines push bone metabolism towards reabsorption and have been observed to induce bone loss in persons with the periodontal disease, pancreatitis, inflammatory bowel disease, and rheumatoid arthritis. An increase in the levels of inflammatory cytokines is also a mechanism by which menopause stimulates bone loss.
Depression: It has been found in various studies that there is a small, but significant association between elevated IL-6 and CRP in depressed patients. At this stage, it is unclear whether inflammation leads to stress or vice versa, and there is data supporting both hypotheses.
Cognitive decline: Several observational studies have linked chronic low-level inflammation in older adults to cognitive decline and dementia, these include vascular dementia and Alzheimer’s disease.
Others: Elevations in circulating inflammatory cytokines are associated with several other conditions, both inflammatory (rheumatoid arthritis, IBD/Crohn’s disease, pancreatitis) and non-inflammatory (anaemia, fibromyalgia, frailty, sarcopenia, cachexia, and muscle wasting). Again, whether inflammation incites these conditions or results from them is unclear and requires further investigation.
It has been found that inflammation, which is the adaptive immune response to tissue injury or infection, plays a central role in metabolism in a variety of organisms. At its most basic level, an acute inflammatory response is triggered by either tissue injury (such as trauma, exposure to heat or chemicals); or infection by viruses, bacteria, parasites, or fungi.
The classic manifestation of acute inflammation is characterised by four cardinal signs:
1) Redness and 2) heat result from the increased blood flow to the site of injury.
3) Swelling results from the accumulation of fluid at the injury site, a consequence of the increased blood flow.
4) Finally, swelling can compress nerve endings near the injury, causing the characteristic pain associated with inflammation. Pain is also important to make the organism aware of the tissue damage.
5) Additionally, inflammation in a joint usually results in impairment of function, which has the effect of limiting movement and forcing rest of the injured joint to aid in healing.
A well-controlled acute inflammatory response has several protective roles:
* It prevents the spread of infectious agents and damage to nearby tissues;
* helps to remove damaged tissue and pathogens, and;
*assists the body’s repair processes.
However, the third type of stimuli, cellular stress and malfunction, triggers chronic inflammation, which, rather than benefiting health, contributes to disease and age-related deterioration via numerous mechanisms.
Mitochondrial dysfunction arises consequent of exposure to exogenous (external environmental toxins, tobacco smoke) and endogenous (internal reactive oxygen species) stressors, and as a result of the ageing process itself. For example, a by-product of mitochondrial energy generation is the creation of free radical molecules. Free radicals can damage cellular structures and initiate a cascade of pro-inflammatory genetic signals that ultimately results in cell death (apoptosis), or worse, uncontrolled cell growth - the hallmark of cancer.
Circulating sugars, primarily glucose and fructose, are culprits as well. When these “blood sugars” come in contact with proteins and lipids a damaging reaction leads to the formation of compounds called advanced glycation end products (AGEs). AGEs bind to the cell-surface receptor called receptor for advanced glycation end products, or RAGE.
Uric acid (urate) crystals, which can be deposited in joints during gouty arthritis. If a patient has elevated levels it might be a risk factor for kidney disease, hypertension, and metabolic syndrome (Oxidised lipoproteins (such as LDL)), a significant contributor to atherosclerotic plaques
Homocysteine, a non-protein-forming amino acid that is a marker and risk factor for cardiovascular disease, and may increase bone fracture risk.
Together, these pro-inflammatory instigators promote a perpetual low-level chronic inflammatory state called para-inflammation. Although it progresses silently, para-inflammation presents a major threat to the health and longevity of all ageing humans. Chronic, low-level inflammation is associated with common diseases including cancer, type II diabetes, osteoporosis, cardiovascular diseases, and others. If it is possible for a patient to target the myriad of physiological variables that can inaugurate an inflammatory response, they can effectively temper chronic inflammation and reduce their risk for inflammatory diseases.
There are several risk factors which increase the likelihood of establishing and maintaining a low-level inflammatory response. These include:
Age: In contrast to younger individuals (whose levels of inflammatory cytokines typically increase only in response to infection or injury), older adults can have consistently elevated levels of several inflammatory molecules, especially IL-6 and TNF-α. These elevations are observed even in healthy older individuals. While the reasoning for this age-associated increase in inflammatory markers is not thoroughly understood, it may reflect cumulative mitochondrial dysfunction and oxidative damage or may be the result of other risk factors associated with age (such as increases in visceral body fat or reductions in sex hormones; see below).
Obesity: Fat tissue is an endocrine organ, which stores and secretes multiple hormones and cytokines into circulation and affecting metabolism throughout the body. Visceral fat cells can produce three times the amount of IL-6 as fats cells elsewhere in the body, and in overweight individuals, may be producing up to 35% of the total IL-6 in the body.
Diet: A diet high in saturated fat is associated with higher pro-inflammatory markers, particularly in diabetic or overweight individuals. The increases in markers of inflammation due to synthetic trans-fats may be more pronounced in individuals that are also overweight.
General dietary over-consumption is a major contributor to inflammation and other detrimental age-related processes in the modern world. Therefore, eating a calorie-restricted diet is an effective means of relieving physiologic stressors. Indeed, several studies show that calorie restriction provides powerful protection against inflammation.
Low sex hormones: Amongst their many roles in biology, sex hormones also modulate the immune/inflammatory response. The cells that mediate inflammation (such as neutrophils and macrophages) have receptors for oestrogens and androgens that enable them to selectively respond to sex hormone levels in many tissues.
Hormone replacement therapy (HRT) may partially exert its protective effects through an attenuation of the inflammatory response. Reductions in the risks of coronary heart disease and inflammatory bowel disease in some individuals, as well as levels of some circulating inflammatory cytokines (including IL-1B, IL-8, and TNF-α) has been observed in some studies of women on hormone replacement therapy.
Smoking: Cigarette smoke contains several inducers of inflammation, particularly reactive oxygen species. Chronic smoking increases production of several pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, IL-8), while simultaneously reducing production of anti-inflammatory molecules. Smoking also increases the risk of periodontal disease, an independent risk factor for increasing systemic inflammation.
Sleep Disorders: Production of inflammatory cytokines (TNF-α and IL-1β) appears to follow a circadian rhythm and may be involved in the regulation of sleep in animals and humans. Disruption of normal sleep can lead to daytime elevations of these pro-inflammatory molecules.
Periodontal disease can produce a systemic inflammatory response that may affect several other systems, such as the heart and kidneys. It is through this mechanism that periodontal disease is thought to be a risk factor for cardiovascular diseases (stimulated by the release of the stress hormone cortisol), both of which are independent causes of inflammation.
Excess Blood Glucose Fuels Inflammatory Fires
When glucose is properly utilised, our cells produce energy efficiently. As cellular sensitivity to insulin diminishes, excess glucose accumulates in our bloodstream. Like the spilled gasoline, excess blood glucose creates a highly combustible environment from which oxidative and inflammatory fires chronically erupt. Excess glucose not used for energy production converts to triglycerides that are either stored as unwanted body fat or accumulate in the blood where they contribute to the formation of atherosclerotic plaque.
As an ageing human, you face a daily onslaught of excess glucose that poses a grave risk to your health and longevity. Surplus glucose relentlessly reacts with your body’s proteins, causing damaging glycation reactions while fuelling the fires of chronic inflammation and inciting the production of destructive free radicals.
Avert Glycation and Inflammation by Controlling Glucose Levels with Green Coffee Bean Extract. Unroasted coffee beans, once purified and standardised, produce high levels of chlorogenic acid and other beneficial polyphenols that can suppress excess blood glucose levels. Human clinical trials support the role of chlorogenic acid-rich green coffee bean extract in promoting healthy blood sugar control and reducing disease risk.
Chronic inflammation or para-inflammation is generally not treated on its own by mainstream physicians. Interventions in conventional medicine are usually only undertaken when the inflammation occurs in association with another medical condition (such as arthritis). Currently, conventional preventive medical approaches to inflammation are limited to the use of CRP to predict cardiovascular disease in high-risk subjects, and the prophylactic use of drugs like aspirin to inhibit the inflammatory cascade linked to thrombosis (uncontrolled blood clotting). Indeed, the potentially asymptomatic nature of low-grade inflammation is such that elevations of pro-inflammatory cytokines may progress undetected for some time, only being discovered after they have had time to cause enough cellular damage to produce disease symptoms. As future studies solidify the association between inflammatory mediators and different diseases, early detection of cytokine aberrations and anti-inflammatory therapy to reduce disease risk may gain more mainstream acceptance.
Your Doctor at Health Renewal will manage chronic inflammation through a consultation and thorough examination. You may be requested to undergo blood tests.
The initial medical consultation at Health Renewal will be approximately 45 minutes. You will have to complete an in-depth questionnaire before the consultation so please arrive 20 minutes prior to your appointment. During the 45 minute consultation, your Health Renewal doctor will obtain a full medical history from you to determine your personal risk. A physical examination will be done after which he/she will decide which blood tests need to be requested from your local pathology laboratory. These results will then be analysed by your Doctor and this will be discussed with you at your follow-up appointments. This will determine whether a definite deficiency exists and you will be advised on your treatment options. These options may range from prescription medications, nutraceuticals, bio-identical hormonal creams or tablets or alternatively to having bio-identical implants or pellets inserted superficially under the skin.
Inflammation itself is not a disease, but is featured, to varying degrees, in adverse health conditions. What follows is a summary of dietary and supplemental approaches to addressing general chronic inflammation and para-inflammation. As many types of general inflammation often occur without additional symptoms, most of the strategies listed below are based on their ability to reduce circulating inflammatory cytokines, the hallmark of the para-inflammatory state
Macronutrients and Energy Balance.
Macronutrient content (particularly the types and levels of carbohydrates and fats) can have a significant effect on the progression of inflammation (as measured by increases in pro-inflammatory markers). Diets with relatively high glycemic index (GI) and glycemic load (GL) have been associated with elevated risk of coronary heart disease, stroke, and type 2 diabetes mellitus, particularly among overweight individuals, and have been associated with modest increases in pro-inflammatory markers in multiple studies. As discussed previously, some dietary fats (particularly saturated and synthetic trans- fats) increase inflammation occurrence, while omega-3 polyunsaturated fats appear to be anti-inflammatory. Since fat tissue (especially abdominal fat) expresses inflammatory cytokines, obesity can be a major cause of low-grade, systemic inflammation. Thus, it is important that total energy intake is proportional to energy expenditure, to avoid the deposition of abdominal fat. Obesity-induced increases in inflammatory cytokines appear to be reversible with fat loss. In a dramatic example, weight loss in a group of 20 severely obese individuals reduced IL-6 by 22% and CRP by almost 50%.
Amongst the most anti-inflammatory nutrients (based on the model and study data) are magnesium, beta-carotene, turmeric (curcumin), genistein, and tea. The most pro-inflammatory included carbohydrates, total- and saturated fat, and cholesterol. The index may provide a useful metric for accessing the overall inflammatory potential of an individual diet.
Exercise. Energy expenditure through exercise lowers multiple cytokines and pro-inflammatory molecules independently of weight loss. While muscle contraction initially results in a pro-inflammatory state, it paradoxically lowers systemic inflammation.
Fiber. In an analysis of 7 studies on the relationship between weight loss and hs-CRP, increased fibre consumption correlated with significantly greater reductions in hs-CRP concentrations.
Micronutrients
Magnesium. There is a significant association between greater dietary magnesium and the lower levels of the inflammation-associated proteins homocysteine and fibrinogen. Magnesium was rated as the most anti-inflammatory dietary factor in the Dietary Inflammatory index, which rated 42 common dietary constituents on their ability to reduce CRP levels based on human and animal experimental and observation data.
Vitamin D. Vitamin D appears to exert anti-inflammatory activity by the suppression of pro-inflammatory prostaglandins, and inhibition of the inflammatory mediator NF-κβ. Vitamin D deficiencies are more common amongst patients with inflammatory diseases (including rheumatoid arthritis, inflammatory bowel disease, systemic lupus erythematosus, and diabetes) than in healthy individuals. They also occur more frequently in populations that are prone to low-level inflammation, such as obese individuals and the elderly.
Vitamin E. Vitamin E functions as an antioxidant in the body. Specifically, vitamin E is incorporated into low-density lipoprotein (LDL) particles and protects them against oxidative damage; it seems to guard against atherosclerosis via other mechanisms as well. The gamma-tocopherol form of vitamin E appears to complement the anti-inflammatory action of alpha-tocopherol. The combination of alpha-tocopherol and gamma-tocopherol supplementation appears to be superior to either supplementation alone on biomarkers of oxidative stress and inflammation.
Other Dietary Factors
Resveratrol and Pterostilbene. The exact mechanism by which resveratrol exerts anti-inflammatory activity has not been established, although it inhibits a variety of pro-inflammatory compounds (cyclooxygenase, TNF-α, IL-1β, IL-6, NF-κβ) in animal models and human cell culture. Resveratrol may be protective against general, low-level para-inflammation as well: when taken with a single high-fat, high-carbohydrate meal (930 kcal), resveratrol (100 mg) prevented the sharp post-meal increases in markers of oxidation and inflammation in a small crossover study of 10 healthy volunteers.
Curcumin. Extensive in vitro and animal studies have examined the effects of curcumin on experimentally-induced inflammatory diseases (atherosclerosis, arthritis, diabetes, liver disease, gastrointestinal disorders, and cancers) and disease markers (lipoxygenase, cyclooxygenase, TNF-α, IL-1β, NF-κβ, and others). Most of the small randomised controlled trials of curcumin have consistently shown patient improvements in several inflammatory diseases, including psoriasis, irritable bowel syndrome, rheumatoid arthritis, and inflammatory eye disease.
Tea polyphenols. The anti-inflammatory effects of green and black tea polyphenols have been substantiated by dozens of in vitro and animal studies. In clinical interventions, black tea appears to be more successful in reducing inflammatory markers than green tea. A 25% reduction in CRP was also observed in a small trial of healthy, non-smoking men consuming a black tea extract (equivalent to 4 cups of tea/day) for 6 weeks. A similar average reduction was observed in a larger study of healthy, individuals at high risk for coronary heart disease, but revealed a more dramatic 40-50% reduction in CRP amongst individuals with the highest starting CRP values (>3 mg/L).
Carotenoids. In the Women’s Health and Aging Study, participants with the highest blood levels of α-carotene and total carotenoids were significantly more likely to have the lower IL-6 levels than participants with low carotenoid levels at the onset of the study. Participants with the lowest blood levels of α- and β-carotene, lutein/zeaxanthin, or total carotenoids were more likely to experience increases in IL-6 over a period of 2 years.
DHEA. Low levels of sex hormones are associated with systemic increases in inflammatory markers; DHEA (dehydroepiandrosterone) is an adrenal steroid hormone, the precursor to the sex steroids testosterone and oestrogen. DHEA is abundant in youth, but steady declines with advancing age and may be partially responsible for age-related decreases sex steroids. In cell culture and animal models, DHEA can suppress inflammatory cytokine activity, in some cases more effectively than either testosterone or oestrogen. Chronic inflammation may itself reduce DHEA levels. DHEA supplementation in elderly volunteers (50 mg/day for 2 years) significantly decreased TNF-α and IL-6 levels, as well as lowered visceral fat mass and improved glucose tolerance (both associated with inflammation).
Fish Oil. This is the best source of the omega-3 fatty acids eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) that can only be synthesised to a limited extent in humans, which is why fish oil supplementation is so critical. Omega-3 fatty acids have been well studied for their prevention of cardiovascular disease and mortality in tens of thousands of patients; the anti-inflammatory effects of omega-3’s contribute to this activity. It has also been successfully proven to improving patient outcomes in scores of studies of other inflammatory diseases, particularly asthma, inflammatory bowel disease, and rheumatoid arthritis.
The association between greater fish oil/omega-3 consumption and reduced systemic inflammation is substantiated by data from several large observational trials. In 855 healthy participants from the Health Professionals Follow-Up Study, intake of omega-3 fatty acids was associated with lower plasma levels of markers of TNF-α activity; interestingly, high intake of both omega-3 and omega-6 fatty acids (which are usually assumed to be pro-inflammatory) was associated with the lowest level of inflammation. The Nurses’ Health Study I cohort of 727 women revealed lower concentrations of inflammatory markers (including CRP and IL-6) amongst those in the top 20% of omega-3 consumption when compared to those who consumed the least amount. In the ATTICA study of over 3000 Greek men and women without any evidence of cardiovascular disease, participants who consumed over 300g of fish per week had, on average, 33% lower CRP, 33% lower IL-6, and 21% lower TNF-α than participants who did not consume fish. In a sample of 5,677 men and women without cardiovascular disease from the Multi-Ethnic Study of Atherosclerosis (MESA) cohort, long-chain omega-3 intake (from fish or supplements) was associated with reduced plasma concentrations of multiple inflammatory markers (including CRP, IL-6, and TNF-α receptor, a measure of TNF-α activity).
N-acetyl cysteine (NAC). Activation of the NF-κB pathway plays a central role in the activation of inflammatory cytokine genes; N-acetyl cysteine inhibits NF-κβ in cell culture, lowering expression of cytokines such as IL-6 and IL-8. Data establishing the effects of NAC on lowering chronic inflammation in humans is limited but shows promise. NAC supplementation for 8 weeks demonstrated the modest, but statistically significant decreases in circulating IL-6 levels in patients with chronic kidney disease. The effects were more pronounced in persons with significant inflammation at the start of the study (as measured by hs-CRP). NAC also reduced markers of systemic inflammation in a small study of patients with burn injuries.
Boswellia. Boswellia serrata (frankincense) is a traditional anti-arthritic in Ayurvedic medicine; its anti-inflammatory properties have been attributed to the specific inhibition of 5-LOX and reduction in the production of pro-inflammatory leukotrienes by boswelic acids, a constituent of the Boswellia gum resin.
Bromelain. The anti-inflammatory activity of the proteolytic enzyme preparation bromelain has been attributed to its ability to reduce COX-2 activity, decrease prostaglandin and thromboxane synthesis, lower circulating fibrinogen levels, and reduce cellular adhesion of pro-inflammatory white blood cells to the sites of inflammation. Another study comparing a standardised commercial enzyme preparation containing bromelain with diclofenac reached the same conclusion. The study reported that the supplement containing bromelain (90 mg, three times daily) to be as effective as diclofenac (50 mg, twice daily) in improving the symptoms of osteoarthritis of the knee. Patients reported comparable reductions in joint tenderness, pain and swelling, and improvement in range of motion at the end of the study. The investigators found bromelain to be as good as diclofenac on a standard pain assessment scale and to be better than the drug in reducing pain at rest.
Reactive oxygen species generated during mitochondrial respiration contribute to inflammation, as outlined above. Ageing individuals are especially susceptible to mitochondria-related oxidative stress since mitochondria become increasingly dysfunctional with age. Taking steps to support mitochondrial integrity and efficiency can help alleviate some of the systemic oxidative and inflammatory burden caused by poorly functioning mitochondria. Two nutrients, coenzyme Q10 (CoQ10) and the pyrrloquinoline quinone (PQQ) are powerful mitochondrial protectants, and studies support an anti-inflammatory role for these compounds.
Pyrroloquinoline quinone is a cofactor for enzymes critically important for cellular energy homeostases and redox balance. Several studies have shown that PQQ exerts a protective effective during circumstantial mitochondrial stress and increased the oxidative load. During periods of limited oxygen supply to the cardiac tissue, a dramatic spike in oxidative stress and subsequent inflammation damages cells; the findings from this animal model indicate that PQQ can stave off this inflammatory cell destruction by preserving mitochondrial efficiency in adverse conditions.
Coenzyme Q10 is an indispensable intermediary in mitochondrial ATP production. Studies have shown that CoQ10 levels are low during inflammatory conditions. In one investigation, patients with septic shock were found to have CoQ10 levels substantially lower than healthy individuals, and, among patients, lower CoQ10 levels correlated with higher levels of an inflammatory mediator called VCAM.
The role of elevated blood sugar and glycation end products in initiating an inflammatory storm has been discussed above. Fortunately, in addition to reducing caloric intake to suppress both fasting and post-meal glucose concentrations, some natural compounds ameliorate the glycation process and may help rein in the sugar-induced inflammatory cascade. Chief among these anti-glycation nutrients are benfotiamine, a member of the B-vitamin family, and carnosine, an amino acid.
Benfotiamine has been used to target diabetic complications since the mid of the 1990’s. More recent evidence continues to support its use as a powerful protector against blood sugar-induced tissue damage. Laboratory experiments have shown that, in addition to blocking glycation reactions, benfotiamine may regulate inflammation more directly by modulating COX and LOX enzyme activity.
Carnosine exerts a range of favourable biochemical effects within the body; it powerfully blunts glycation reactions and eases oxidative stress. In addition, several experiments have revealed a marked ability of carnosine to suppress inflammation in various cell types.
A multi-gene DNA test can routinely be added to assessment of
It includes analysis of variation in clinically useful genes that may contribute to abnormal cholesterol levels,
Some of these abnormalities contribute to the development of type II diabetes, obesity and hypertension. Oxidative stress, detoxification of carcinogens and oestrogen exposure are also important considerations in this context.
This pathology supported genetic test is performed in conjunction with assessment of any food allergy or intolerances known to be associated with many chronic disorders. The results of the genetic test are combined with clinical indicators and lifestyle factors to identify a combination of risk factors that may lead to disease development or the progression if left untreated.
For all health conditions, the nutraceuticals are individually tailored by the Health Renewal Doctor. The doctor will decide- based on your history, physical examination and blood tests what would be the best for you and your specific needs and/or deficiencies. It cannot be overemphasised that one must not self-medicate. Self-Medicating is done when a person takes prescription medication or nutraceuticals on their own without a doctor's supervision and/or consent. By not having a physical examination and blood testing done by a qualified and practising integrative medical practitioner, you could be not treating vital deficiencies or conditions such as elevated blood pressure, high sugar level, high stress levels (that can lead to adrenal burnout ) and high blood clotting factors that could lead to heart attacks and stroke. In addition, the aggressive program of dietary supplementation should not be launched without the supervision of a qualified physician. Several of the nutrients suggested in this protocol may have adverse effects. There is no single supplement prescribed to clients as there is no magic bullet that can support all the essential nutrients that one's body needs. Today's food is not functional and we need to supplement in order to maintain optimal bodily functions and nutrition.
Make an appointment to consult with your Health Renewal Doctor who is an integrative doctor and he or she will assist you in determining your risk factors and how best to prevent any problems or conditions that you may be susceptible to. The importance of early management of any condition cannot be overstated. Once certain conditions set in and damage to organs occurs, complete recovery may be difficult to attain. Best results for prevention and longevity is early detection of a possible problem combined with conventional treatments, nutritional supplements and a healthy diet and lifestyle.
The initial medical consultation at Health Renewal will be approximately 45 minutes. As this is a prolonged medical consultation, the initial consultation fee will be R 975 on arrival (for non-loyalty programme members) you will have to complete an in-depth questionnaire before the consultation so please arrive 20 minutes before the time. During the 45 minute consultation, your Health Renewal doctor will obtain a FULL medical history from you to determine your personal risk. A physical examination will be done after which the Doctor will decide which blood tests need to be requested from your local pathology laboratory. If you have a medical aid, these should be able to be claimed as well.
Once your blood results are received, they will then be analysed by your Health Renewal doctor who will begin working on a unique prescription plan for you with the compounding pharmacy. At your pre-scheduled second appointment 2 weeks later, the results and examination findings will be discussed with you. This will determine what abnormalities or deficiencies exist and you will be advised on your treatment options. These options may range from prescription medications, nutraceuticals, bio-identical hormonal creams or tablets or alternatively to having bio-identical implants or pellets inserted.
In office treatments such as carboxytherapy may also be recommended for certain conditions such as hair loss, erectile dysfunction ED, menopause or PMS. If you need to lose weight our Renewal Institute Diet may be recommended. All these recommendations will be summarised on a sheet or print out which you can take home with you. The nutraceuticals offered at Health Renewal are of superior quality (Solgar) and are not rancid nor contain Hg (mercury ) or PCB'S (which is very important for Omega 3 Essential fatty acids EFA's). They are also free of gluten, preservatives, wheat, dairy, soy, yeast, sugar, artificial flavour, sweetener and colour. We have a great professional team made up of doctors, trained and registered nurses and therapists to support you at any time.
1. You are kindly requested to bring any supplements that you are currently taking, along to your consultation. The doctor can check the ingredients in this and take it into account when prescribing a treatment plan for you.
2. Also, if you have had any blood work done in the past 6 months, please bring the results along to the consultation. Should you not be in possession of the hard copies, please request these results from the lab you visited. Usually, your ID number is sufficient.
Depending on the exact prescription given, you may be required to return to the doctor within 1-4 months’ time, in order to ensure optimum hormone levels are achieved. This will be determined by a repeat blood test and may be requested by your Health Renewal doctor.
You should ensure that you are current with your gynaecological visits/breast exams/mammograms (for female patients) and prostate exams (for male patients) as recommended by your GP/gynaecologist.
Depending on which form of supplementation you and your Health Renewal Doctor have decided on, one could expect to follow up with your physician from anything between every 3 months to once every 6 months.
General Support
Magnesium: 100 – 800 elemental milligrams of highly-absorbable magnesium
Vitamin D: 5000 – 8000 IU daily (depending on blood test results; optimal blood levels are between 50 and 80 ng/mL)
Vitamin A: 500 IU acetate and 4500 IU beta-carotene daily
Natural Vitamin E: 100 – 400 IU alpha-tocopherol and 200 mg gamma-tocopherol daily
Fish oil (with olive polyphenols and sesame lignans): providing 1400 mg EPA and 1000 mg DHA daily
Zinc: 30 mg daily
Selenium: 200 mcg daily
DHEA: 15 – 25 mg daily for women, and 25 – 75 mg daily for men (depending on blood test results)
Antioxidants
Trans-resveratrol: 100 – 500 mg daily
Trans-pterostilbene: 0.5 – 50 mg daily
Green tea extract, standardized to 98% polyphenols: 725 – 1450 mg daily
Black tea extract, standardized to 25% theaflavins: 350 mg daily
N-Acetylcysteine: 600 – 1200 mg daily
Mechanism-Specific Support
Curcumin (as highly absorbed BCM-95®): 400 – 800 mg daily
Boswellia serrata extract (as highly absorbed AprèsFlex™), standardized to 20% AKBA: 100 mg daily
Bromelain (enteric coated): 500 – 1000 mg daily
Optimizing Glucose Levels and Targeting Advanced Glycation End Products
Green coffee bean extract, standardized to 50% chlorogenic acid: 200 – 400 mg before each meal, up to three times daily
Benfotiamine: 150 – 1000 mg daily
L-carnosine: 500 – 1500 mg daily
Supporting Mitochondrial Function
Pyrroloquinoline quinone: 10 – 20 mg daily
CoQ10 (as ubiquinol): 100 – 200 mg daily
The importance of early management of any condition cannot be overstated. Once certain conditions set in and damage to organs occurs, complete recovery may be difficult to attain. Best results for prevention and longevity is early detection of a possible problem combined with conventional treatments, nutritional supplements and a healthy diet and lifestyle.
Here are ten quotes from great thinkers to challenge, motivate and inspire us to exercise, eat right and live healthier lives: Health and intellect are the two blessings of life.
