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The Skinny On Skin: Zap The Zits and More

fighting-pimplesIt seems to happen just when the prom is a week away, or on the day before your date with the most popular gal or guy in school.   You get a pimple big enough to get its own name, like Everest or Matterhorn.  What can you do about it?  Could it have been prevented?  If you’re a teenager reading this, and suffer from acne, read closely as there may be an answer to your dilemma. If you’re a parent, maybe you could pass this on.

Acne has a bunch of names, but we bet you could add your own.  Basically, it’s an inflammation of the sebaceous glands, those that make sebum, the stuff that acts as a lubricant for the hair and skin and offers some protection against attackers like bacteria.  The “stuff” consists of fat, keratin, and cellular material that ooze from the follicle, the hair tube to which the sebaceous gland is attached.  As skin cells lining the follicle die off, they are pushed out by a growing hair.  Sometimes too much keratin interrupts this process and the dead skin cells stick together, clogging up the works.  This is how acne starts.  That thing we call a zit or blackhead is known as a comedone.  This word has nothing to do with comedy—there’s nothing funny about it, especially if it’s yours.

Acne is considered a normal response to abnormal levels of the male hormone testosterone.  Women may experience moderate acne due to hormonal changes associated with female health issues that include pregnancy, the use of birth control pills, and menstruation.   Not that this will make you feel any better, but four out of five people between ages twelve and twenty-four will get acne at least once.  As with most horrendous teenage afflictions, there are risk factors for acne, including some you can control and some you can’t.  You might be able to control bacterial growth by frequent and careful washing and rinsing.   You most assuredly can avoid using steroids to bulk up for a sport, and you can avoid skin irritation from scratching or the constant contact of a telephone against your face.  Genes and overproduction of sebum and hormone activity are not under your direct control.  Stress may or may not be, depending on whether or not you share living space with the Wicked Witch or the kindly Wiz.

Treatment for acne is generally based on reducing skin oil production, hastening skin cell turnover, fighting bacterial infection, or all three at the same time.  Topical treatments can do that, sometimes over-the-counter, sometimes by prescription.  Antibiotics, either rub-on or by-mouth, require an Rx.  For acne that fails to respond to other treatment, there’s an oral drug called Accutane, which is the atomic bomb of acne treatments, with a list of precautions, interactions and side effects long enough to choke a giraffe.  Recently, a slightly less offensive medication, a topical formulation called clindamycin phosphate, was matched head-to-head with an all-natural preparation made from vitamin B3 (as nicotinamide) and phosphatidylcholine (PC).

Remember, previously where we said keratin can clog up the works?  That’s termed hyperkeratinization.  That unwelcome activity was found to be reversed and normalized by using topical linoleic-acid-rich PC combined with nicotinamide’s anti-inflammatory character.  Contrasted to clindamycin in a 12-week, double-blind, randomized study, the PC/B3 compound was better tolerated and slightly superior in outcome (Morganti, 2011).

For more than a few years science has been concerned that bacteria are learning to become resistant to medicine’s barrage of chemical agents.  Concurrently, it’s been accepted that natural villains do not generally grow immune to natural heroes.  In the matter of acne, this was realized about nicotinamide more than a decade ago.  The emergence of resistant pathogens led researchers to look in a direction away from systemic and topical synthetic antimicrobials in the treatment of this condition.  Topical nicotinamide as a 4% gel was discovered to be a potent anti-inflammatory agent without the risk of bacterial resistance and, in fact, showed an 82% symptom improvement rate over clindamycin’s 68% (Shalita, 1995).  But wait, there’s a whole lot more to this.  In order for topical treatments to be effective, they have to get through the skin’s horny layer, the stratum corneum, without causing damage to tissue.  What natural substance can do this without unwanted side effects?  Phosphatidylcholine!

The prime phospholipid from which we are made, phosphatidylcholine renders cell membranes vibrant and alive, an activity lacking which we’d all succumb.  But it’s not only a stanchion; it’s also an escort.  PC helps desirable materials to permeate the skin’s stratum corneum and deliver healing, whether all natural or man-made, the former being preferred.  The higher the concentration of PC, the higher the efficacy of the escorted material (Kim, 2002).  While this holds true for nicotinamide, it also holds for drugs.  Indomethacin is an Rx non-steroidal anti-inflammatory drug (NSAID) used to address the discomfort of arthritis, tendinitis, and bursitis and like conditions.  It’s usually taken orally, but an Indomethacin topical gel made with liquid paraffin and mixed with PC was found to be considerably more effective at crossing the skin’s horny layer than the product that omitted the PC (Fujii, 2001).  Compared to conventional petroleum-based carriers of topical interventions, PC-based carriers improve the effectiveness of drugs used for skin cancer, as well (Romagosa, 2000).

PC as an oral supplement has long been known to attenuate serum cholesterol. In combination with niacin therapy for elevated cholesterol, PC is astounding.  No one ever dreamed that it could pass through the skin and have a similar effect.  The University of Miami’s School of Medicine looked at PC through a creative eye, and applied it topically to the shaved backs of rabbits that were bred to develop hypercholesterolemia and atherosclerotic lesions.  After two weeks’ treatment, investigators noted reduced levels of serum cholesterol and LDL, accompanied by less severe signs of atherosclerosis in the aorta (Hsia, 1996).

The incredible characteristics of real phosphatidylcholine—the kind that forms a liposome—are easier to realize than you might think.  Check out www.bodybio.com for more PC facts.

References

Berbis P, Hesse S, Privat Y.
Essential fatty acids and the skin
Allerg Immunol (Paris). 1990 Jun;22(6):225-31.

Downing DT, Stewart ME, Wertz PW, Strauss JS.
Essential fatty acids and acne.
J Am Acad Dermatol. 1986 Feb;14(2 Pt 1):221-5.

Fujii M, Shiozawa K, Watanabe Y, Matsumoto M.
Effect of phosphatidylcholine on skin permeation of indomethacin from gel prepared with liquid paraffin and hydrogenated phospholipid.
Int J Pharm. 2001 Jul 3;222(1):57-64.

Godin AM, Ferreira WC, Rocha LT, Seniuk JG, Paiva AL, Merlo LA, Nascimento EB Jr, Bastos LF, Coelho MM.
Antinociceptive and anti-inflammatory activities of nicotinamide and its isomers in different experimental models.
Pharmacol Biochem Behav. 2011 Oct;99(4):782-8. Epub 2011 Jul 8.

Makiko Fujii, Kumi Shiozawa, Yoichi Watanabe, Mitsuo Matsumoto
Effect of phosphatidylcholine on skin permeation of indomethacin from gel prepared with liquid paraffin and hydrogenated phospholipid
International Journal of Pharmaceutics.  Vol 222, Iss 1, 3 July 2001, Pages 57–64

Hsia SL, He JL, Nie Y, Fong K, Milikowski C.
The hypocholesterolemic and antiatherogenic effects of topically applied phosphatidylcholine in rabbits with heritable hypercholesterolemia.
Artery. 1996;22(1):1-23.

Kanmaz T, Karakayali H, Sakallioglu AE, Ozdemir BH, Haberal M.
Polyunsaturated phosphatidylcholine protects against wound contraction in experimental skin burn injury.
J Invest Surg. 2004 Jan-Feb;17(1):15-22.

Kim C, Shim J, Han S, Chang I.
The skin-permeation-enhancing effect of phosphatidylcholine: caffeine as a model active ingredient.
J Cosmet Sci. 2002 Nov-Dec;53(6):363-74.

McCusker MM, Grant-Kels JM.
Healing fats of the skin: the structural and immunologic roles of the omega-6 and omega-3 fatty acids.
Clin Dermatol. 2010 Jul-Aug;28(4):440-51

Morganti P, Berardesca E, Guarneri B, Guarneri F, Fabrizi G, Palombo P, Palombo M.
Topical clindamycin 1% vs. linoleic acid-rich phosphatidylcholine and
nicotinamide 4% in the treatment of acne: a multicentre-randomized trial.

Int J Cosmet Sci. 2011 Oct;33(5):467-76.

Romagosa R, Saap L, Givens M, Salvarrey A, He JL, Hsia SL, Taylor JR.
A pilot study to evaluate the treatment of basal cell carcinoma with 5-fluorouracil using phosphatidyl choline as a transepidermal carrier.
Dermatol Surg. 2000 Apr;26(4):338-40.

Shalita AR, Smith JG, Parish LC, Sofman MS, Chalker DK.
Topical nicotinamide compared with clindamycin gel in the treatment of inflammatory acne vulgaris.
Int J Dermatol. 1995 Jun;34(6):434-7.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

The Skinny On Skin

Summer beautyUnlike other organs of the body, skin nutrition can be enhanced by “direct deposit” through topical application of micronutrients, which can complement dietary acquisition and result in a stronger, healthier barrier to the world. Did you know that, when you look at a person, you are looking at dead skin? That would be the horny, keratinized outer layer called the stratum corneum. Keratin is a protein that helps to keep skin hydrated by preventing water evaporation. You might recognize it as the major component of wool, nails, rhino horns, and quill pens. The cells of the stratum corneum can also absorb water, which explains the puffiness and wrinkling you get in your fingers from sitting in the tub too long. Be glad this doesn’t happen all over. Sometimes, when your skin gets dry and itchy, you can see flakes of it when you scratch. That is the stratum corneum, part of the epidermis, which also contains the skin pigmentation chemical called melanin. Since people who look at you are seeing the walking dead, you might as well try to make it at least a little bit attractive.

Dry skin can be caused by harsh detergents and soaps, and by nutritional deficiencies, especially of essential fatty acids. Diet aside, at least for now, topical treatments can help to keep skin moist and pliable. There are no blood vessels in the epidermis to deliver nutrients to the stratum corneum, which usually prevents the passage of many types of molecules to layers below. Sometimes, though, a compound will pass through. Changes in temperature, air flow and humidity can pull water away from the skin and interrupt its integrity. If ignored, this can lead to more serious concerns, including cell damage and inflammation that perpetuate the condition. An important strategy is to address dry skin by maintaining the lipid components of what is termed the natural moisturizing factor.

The outer layers of the epidermis receive less nutritional support than underlying cells, hence the slowness and limitation of dietary interventions to offer positive effects. On the bright side, concentrations of nutrients in the skin can eventually be met through oral avenues. On the other hand, topical application may be more efficient, especially to ameliorate the ravages of photodamage (Pinell, 2003) (Zussman, 2010). Long before other insults were considered, poor nutrition was associated with changes in skin appearance, with the vitamin C deficit known as scurvy being among the first to be identified. Later associations, such as pellagra and ariboflavinosis, were found to be correctible through diet.

The topical use of micronutrients is a relatively new area of study (Boelsma, 2001). Much has been discussed and publicized about vitamins C, D, and E for skin health. Fatty acids have also been part of the conversation, and ceramides are slowly coming into the limelight (Coderch, 2003) (Guillou, 2011). This is warranted because the stratum corneum contains high levels of ceramides, constituting as much as half the total lipids, where they serve as a kind of glue that holds surface skin cells together.

But a not-so-new-kid on the block is gaining recognition for participation in the parade that leads to rescue of failing skin—the B-vitamins, 3 and 5. Nicotinamide (B3) is the amide of nicotinic acid, which is the form of niacin able to lower cholesterol and to cause flushing.  Nicotinamide is also called niacinamide, known to reduce glucose levels. Metabolically, nicotinamide is convertible to nicotinic acid. Though pharmacologically different, niacin/nicotinic acid and nicotinamide/niacinamide have the same vitamin activity. In a Japanese study conducted about a decade ago, it was found that topical nicotinamide is able to improve the permeability barrier of skin by stimulating the synthesis of ceramides, free fatty acids and cholesterol, with a subsequent decrease in transepidermal water loss (Tanno, 2000).

Not to be left out of the mix, panthenol likewise lends its magic to a topical lotion. Panthenol is the alcohol analog of pantothenic acid, also known as vitamin B5, that acts as a provitamin since it is quickly converted to vitamin B5. Only the D- form is biologically active, but both it and the L- form have moisturizing properties. In cosmetics, it may appear as DL-panthenol. Combined with niacinamide, this nutrient was shown to reduce a few obvious signs of aging skin, notably hyperpigmentation and redness. In a blinded study carried out in India, researchers found that subjects who applied such a lotion to the face daily for ten weeks experienced a significant reduction in redness and hyperpigmentation, an improvement in skin tone evenness, and positive effects on skin texture (Jerajani, 2010). Even in the absence of B5, the B3 application (niacinamide) alone was able to reduce the same negative features while simultaneously diminishing fine lines and wrinkles (Bissett, 2005) (Kawada, 2008).

Traditionally, vitamins have played the role of co-enzymes. You still need to eat food to give the vitamins something to work with. Several vitamins, however, assume the role of endocrine mimics. Biotin is one of these. Critical to carboxylation—replacing a hydrogen atom (H) with a carboxyl group (COOH), as in the oxidation of products that result from the decomposition of carbohydrates, fats and proteins—biotin also induces epidermal cell differentiation (Bolander, 2006), a process that helps to make new cells. This is especially noticeable in the health of fingernails and animals’ hooves, which become increasingly brittle and friable in the absence of biotin (Colombo, 1990) (Hochman, 1993).

We all know that exposure to the sun helps to make vitamin D. But we also know that too much exposure can cause the skin problems we’re trying to prevent or to rectify. The sun’s ultraviolet light is part of the invisible band of radiation. Most (~95%) of the UV that reaches the earth is the lower-frequency, longer-length UVA, sometimes called black light, that penetrates more deeply into the skin than UVB, but is less intense. UVA is the tanning ray that plays a major role in photoaging. UVB is responsible for sunburn and reddening, damaging the superficial layers of the epidermis. Both are culprits. Nicotinamide has been involved in cellular energy restoration after UV irradiation and is found to be immune protective, but riboflavin—vitamin B2—has similar virtue in that it is vital to cellular energy metabolism. Scientists who speculated that B2 could offer immune protection as well as B3 after insult by UV light were correct. Topical riboflavin protected against both wavebands (Diona, 2010) (Yoshikawa, 1999), and oral riboflavin can prevent dermatitis (Lo, 1984).

Taking a single B vitamin orally may have undesirable results; taking it as part of the entire complex, or adding it to the complex, is not a concern. Deficiency of B vitamins can be related to acne, cracked lips, dryness, wrinkles and an uneven complexion, among other dermatological (and metabolic) involvements. Avoiding these issues may be as easy as taking a supplement or finding a fortified lotion.

References

Bissett DL, Miyamoto K, Sun P, Li J, Berge CA.
Topical niacinamide reduces yellowing, wrinkling, red blotchiness, and hyperpigmented spots in aging facial skin.
Int J Cosmet Sci. 2004 Oct;26(5):231-8. doi: 10.1111/j.1467-2494.2004.00228.x.

Bissett DL, Oblong JE, Berge CA.
Niacinamide: A B vitamin that improves aging facial skin appearance.
Dermatol Surg. 2005 Jul;31(7 Pt 2):860-5; discussion 865.

Boelsma E, Hendriks HF, Roza L.
Nutritional skin care: health effects of micronutrients and fatty acids.
Am J Clin Nutr. 2001 May;73(5):853-64.

Bolander FF.
Vitamins: not just for enzymes.
Curr Opin Investig Drugs. 2006 Oct;7(10):912-5.

Coderch L, López O, de la Maza A, Parra JL.
Ceramides and skin function.
Am J Clin Dermatol. 2003;4(2):107-29.

Colombo VE, Gerber F, Bronhofer M, Floersheim GL.
Treatment of brittle fingernails and onychoschizia with biotin: scanning electron microscopy.
J Am Acad Dermatol. 1990 Dec;23(6 Pt 1):1127-32.

Diona L. Damian, Yasmin J. Matthews, Gary M. Halliday
Topical riboflavin attenuates ultraviolet B- and ultraviolet A-induced immunosuppression in humans
Photodermatology, Photoimmunology, & Photomedicine. Apr 2010; 26(2): 66-69

Guillou S, Ghabri S, Jannot C, Gaillard E, Lamour I, Boisnic S.
The moisturizing effect of a wheat extract food supplement on women’s skin: a randomized, double-blind placebo-controlled trial.
Int J Cosmet Sci. 2011 Apr;33(2):138-43. doi: 10.1111/j.1468-2494.2010.00600.x.

Hochman LG, Scher RK, Meyerson MS.
Brittle nails: response to daily biotin supplementation.
Cutis. 1993 Apr;51(4):303-5.

Jerajani HR, Mizoguchi H, Li J, Whittenbarger DJ, Marmor MJ.
The effects of a daily facial lotion containing vitamins B3 and E and provitamin B5 on the facial skin of Indian women: a randomized, double-blind trial.
Indian J Dermatol Venereol Leprol. 2010 Jan-Feb;76(1):20-6. doi: 10.4103/0378-6323.58674.

Kawada A, Konishi N, Oiso N, Kawara S, Date A.
Evaluation of anti-wrinkle effects of a novel cosmetic containing niacinamide.
J Dermatol. 2008 Oct;35(10):637-42. doi: 10.1111/j.1346-8138.2008.00537.x.

Lacroix B, Didier E, Grenier JF.
Role of pantothenic and ascorbic acid in wound healing processes: in vitro study on fibroblasts.
Int J Vitam Nutr Res. 1988;58(4):407-13.

Lo CS.
Riboflavin status of adolescents in southern China. Average intake of riboflavin and clinical findings.
Med J Aust. 1984 Nov 10;141(10):635-7.

Mori K, Ando I, Kukita A.
Generalized hyperpigmentation of the skin due to vitamin B12 deficiency.
J Dermatol. 2001 May;28(5):282-5.

New D, Eaton P, Knable A, Callen JP.
The use of B vitamins for cutaneous ulcerations mimicking pyoderma gangrenosum in patients with MTHFR polymorphism.
Arch Dermatol. 2011 Apr;147(4):450-3. doi: 10.1001/archdermatol.2011.77.

Pinnell SR.
Cutaneous photodamage, oxidative stress, and topical antioxidant protection.
J Am Acad Dermatol. 2003 Jan;48(1):1-19; quiz 20-2.

Rajendran Kannan, MB BS MD and Matthew Joo Ming Ng, MB BS M Med Dip OccMed FCFPS
Cutaneous lesions and vitamin B12 deficiency
An often-forgotten link

Can Fam Physician. 2008 April; 54(4): 529–532.

Tanno O, Ota Y, Kitamura N, Katsube T, Inoue S.
Nicotinamide increases biosynthesis of ceramides as well as other stratum corneum lipids to improve the epidermal permeability barrier.
Br J Dermatol. 2000 Sep;143(3):524-31.

Yoshikawa K.
Vitamin and dermatology
Nihon Rinsho. 1999 Oct;57(10):2385-9.

Zussman J, Ahdout J, Kim J.
Vitamins and photoaging: do scientific data support their use?
J Am Acad Dermatol. 2010 Sep;63(3):507-25.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Diabetes Management: Dietary Interventions

diabetes-mangmntDiabetes, the word, is loosely derived from a Greek translation of “one that straddles,” probably referring to a person who urinates frequently. You already know this is considered a metabolic disease of several types, marked by frequent urine discharge, persistent thirst, and the inability to process sugars in the diet due to a decrease in, or absence of, insulin production. There also may be target tissue insulin resistance. Type 1 diabetes mellitus is one of the two major types. Here, the symptoms arise abruptly, often in early adolescence, and the person relies on exogenous insulin to sustain life. Onset may occur at any age, though. Among other miseries, type 1 affects blood vessel health (especially the tiny ones), and manifests in the retina, kidneys, and the underlying connective layer of arterioles. Type 2 diabetes often strikes between ages thirty and forty, with gradual onset that shows few symptoms of metabolic disturbance, at least not right away. With good fortune and careful management, there may be no need for exogenous insulin; diet and perhaps oral hypoglycemic medications can do the trick. Insulin response in type 2 is delayed or reduced, but insulin secretion is not necessarily absent. In this disorder blood vessels of various sizes are affected, particularly the large ones. This can lead to premature atherosclerosis, sometimes followed by myocardial infarction and stroke. Neither of these types of diabetes is to be taken lightly. There is also a third type of diabetes, diabetes insipidus, usually caused by hormone or kidney anomalies.

You might have heard people refer to themselves as having “a touch of diabetes.”  That’s the equivalent of being a little bit pregnant. Either you are, or you aren’t. Maybe you’ll hear folks say their sugar is “a little high.”  Either expression hints that diabetes is not a serious matter. That is wrong. Managing diabetes may not be the easiest thing in the world, but it certainly is achievable, and in the long run it’s well worth the effort. When your blood sugar is normal, you feel better—you have more energy, are less tired and thirsty, have fewer skin or bladder infections, you heal faster, and you have fewer problems with your vision, teeth and feet. Taking care of yourself will avoid heart attack and stroke, the possibility of blindness, nerve damage that causes tingling and numbness in hands and feet, kidney disease that may kill you, and gum disease that causes tooth loss. Hmm, this is serious business.

Unfortunately, the body is not modular in that an organ can be removed and replaced when the warranty is near expiration. It’s not like rotating tires. Even artificial joints don’t come with grease fittings. We have to make parts last as long as possible, despite that some can be replaced…an uncomfortable though to many of us. Prevention is still the best cure. Diabetes can lead to cardiovascular damage. Yes, eyesight and nerves can be damaged, too, but space restricts us to one topic at a time. Changes in the body don’t necessarily happen independently. The cycle of progressive vascular damage from diabetes affects the heart. Changing how we eat can manage glucose levels and prevent heart disease.  One dietary technique follows the glycemic index (GI), which is a measure of how fast blood sugar rises in response to a certain food.  The index estimates how much a gram of carbohydrate elevates blood sugar after consumption, relative to consumption of pure glucose, which is given an index value of 100. Subjects with diabetes managed only by a diet focusing on optimal glycemic control were found to have reduced postprandial glucose levels, accompanied by lower markers of inflammation, notably C-reactive protein (CRP), and improved lipid panels (Wolever, 2008). From time to time, meta-analyses are employed to examine relationships among disease-causing variables. Scrutinizing the GI relationship to CVD, Australian scientists, whose colleagues are credited with designing the GI, discovered a reduction in the risk for cardiovascular disease among diabetes patients who complied with the low GI regimen (Barclay, 2008). The low GI has such potential in the management of chronic disease that those who are morbidly obese may find heart-healthy value in following the plan (Ebbeling, 2005). Even in cases where diabetes is poorly controlled, adhering to the low GI diet has merit when combined with reduced carbohydrate intake in modulating CVD risk factors, including glycated hemoglobin, called HbA1c ( Afaghi, 2012) (Eskesen, 2013) (Zhang, 2012).  Glycated hemoglobin is formed through a non-enzyme pathway when hemoglobin is exposed to high plasma levels of glucose. Glycation forms end products that cause extreme oxidative stress on the body, affecting nearly every cell and molecule. The advanced glycation end products, termed AGE’s, increase vascular permeability, inhibit vascular dilation (and elevate blood pressure), interfere with nitric oxide production (which allows blood vessels to dilate), oxidize LDL, and excite excretion of cytokines. These pathological states invite cardiac entanglement, but can be managed successfully through dietary modification.

The Mediterranean Diet has been touted for its cardiovascular benefits, but little attention has been paid to its effect on diabetes issues.  This diet is a relative newcomer to us, although it’s been a way of life in the Mediterranean for years, generally in the less opulent areas of southern Italy, parts of Greece and a few islands. Despite being called such, this diet is not typical of the entire area. For instance, wine is avoided by the Muslims of the region, and butter, lard and other animal fats comprise part of the cuisine of various indigenous groups. One thing that is easily identifiable about this regional lifestyle is ambulation—everybody walks everywhere. You know very well that accounts for a lot. The diet is abundant in plant foods. Fruit is dessert, as opposed to the sugary stuff Americans eat. The main fat is olive oil; cheese and yogurt are the chief dairy products; red meat is more an accoutrement than a feature. Legumes, unrefined non-GMO cereals, huge amounts of fruits and vegetables, moderate consumption of fish and poultry, and little saturated fat are the norm.

A cohort of more than thirteen thousand Spanish university graduates was followed for four years to assess an association of diet and diabetes. Participants who followed the Mediterranean protocol had a lower risk of disease (Martinez-Gonzalez, 2008) (Dominguez, 2012). There was no beating about the bush in this report. The conclusion was stated with conviction. At the same time, it was noted that seduction by the typical Western diet of fast and prepared foods leads to increases in cardiovascular and metabolic complications (Tarabusi, 2010).

In all the controlled trials reviewed in recent years, those that featured low GI, low carbohydrate and Mediterranean diets all led to greater improvement in glycemic control, with the Mediterranean having the most profound influence on both glucose control and weight loss, enhanced by increases in HDL (Ajala, 2013). Reduction in markers of inflammation and decreases in AGE’s are among the goals in the management of blood glucose and coronary health. AGE’s affect the physiological profiles of proteins by creating cross-links, and they induce vascular dysfunction by stiffening blood vessels and myocardial tissue. Keeping HbA1c where your doctor wants it will keep you alive long enough to be chastised for decades.

References

Abiemo EE, Alonso A, Nettleton JA, Steffen LM, Bertoni AG, Jain A, Lutsey PL.
Relationships of the Mediterranean dietary pattern with insulin resistance and diabetes incidence in the Multi-Ethnic Study of Atherosclerosis (MESA).
Br J Nutr. 2012 Aug 30:1-8.

Afaghi A, Ziaee A, Afaghi M.
Effect of low-glycemic load diet on changes in cardiovascular risk factors in poorly controlled diabetic patients.
Indian J Endocrinol Metab. 2012 Nov;16(6):991-5.

Ajala O, English P, Pinkney J.
Systematic review and meta-analysis of different dietary approaches to the management of type 2 diabetes.
Am J Clin Nutr. 2013 Mar;97(3):505-16.

Anastasios S Dontas, Nicholas S Zerefos, Demosthenes B Panagiotakos, and Dimitrios A Valis
Mediterranean diet and prevention of coronary heart disease in the elderly
Clin Interv Aging. 2007 March; 2(1): 109–115.

Barclay AW, Petocz P, McMillan-Price J, Flood VM, Prvan T, Mitchell P, Brand-Miller JC.
Glycemic index, glycemic load, and chronic disease risk–a meta-analysis of observational studies.
Am J Clin Nutr. 2008 Mar;87(3):627-37.

Bédard A, Riverin M, Dodin S, Corneau L, Lemieux S.
Sex differences in the impact of the Mediterranean diet on cardiovascular risk profile.
Br J Nutr. 2012 Oct 28;108(8):1428-34.

Chiu CJ, Liu S, Willett WC, Wolever TM, Brand-Miller JC, Barclay AW, Taylor A.
Informing food choices and health outcomes by use of the dietary glycemic index.
Nutr Rev. 2011 Apr;69(4):231-42.

Domínguez LJ, Bes-Rastrollo M, de la Fuente-Arrillaga C, Toledo E, Beunza JJ, Barbagallo M, Martínez-González MA.
Similar prediction of decreased total mortality, diabetes incidence or cardiovascular events using relative- and absolute-component Mediterranean diet score: The SUN cohort.
Nutr Metab Cardiovasc Dis. 2012 Mar 6.

Due A, Larsen TM, Mu H, Hermansen K, Stender S, Astrup A.
Comparison of 3 ad libitum diets for weight-loss maintenance, risk of cardiovascular disease, and diabetes: a 6-mo randomized, controlled trial.
Am J Clin Nutr. 2008 Nov;88(5):1232-41.

Ebbeling CB, Leidig MM, Sinclair KB, Seger-Shippee LG, Feldman HA, Ludwig DS.
Effects of an ad libitum low-glycemic load diet on cardiovascular disease risk factors in obese young adults.
Am J Clin Nutr. 2005 May;81(5):976-82.

K. Eskesen, M. T. Jensen, S. Galatius, H. Vestergaard, P. Hildebrandt, J. L. Marott,
J. S. Jensen
Glycated haemoglobin and the risk of cardiovascular disease, diabetes and all-cause mortality in the Copenhagen City Heart Study
Journal of Internal Medicine. Vol 273, Iss 1, pp 94–101, January 2013

Hartog JW, Voors AA, Bakker SJ, Smit AJ, van Veldhuisen DJ.
Advanced glycation end-products (AGEs) and heart failure: pathophysiology and clinical implications.
Eur J Heart Fail. 2007 Dec;9(12):1146-55.

Konstantinidou V, Covas MI, Sola R, Fitó M.
Up-to date knowledge on the in vivo transcriptomic effect of the Mediterranean diet in humans.
Mol Nutr Food Res. 2013 Feb 18. doi: 10.1002/mnfr.201200613. [Epub ahead of print]

Kuhlmann M., Levin N.
Interaction between Nutrition and Inflammation in Hemodialysis Patients. in “Cardiovascular Disorders in Hemodialysis”
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Lagiou P, Sandin S, Weiderpass E, Lagiou A, Mucci L, Trichopoulos D, Adami HO.
Low carbohydrate-high protein diet and mortality in a cohort of Swedish women.
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Lagiou P, Sandin S, Lof M, Trichopoulos D, Adami HO, Weiderpass E.
Low carbohydrate-high protein diet and incidence of cardiovascular diseases in Swedish women: prospective cohort study.
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Lajous M, Boutron-Ruault MC, Fabre A, Clavel-Chapelon F, Romieu I.
Carbohydrate intake, glycemic index, glycemic load, and risk of postmenopausal breast cancer in a prospective study of French women.
Am J Clin Nutr. 2008 May;87(5):1384-91.

Talya Lavi, RD, Avraham Karasik, MD, Nira Koren-Morag, PHD, Hannah Kanety, PHD,
Micha S. Feinberg, MD, Michael Shechter, MD, MA
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