Nutrition - Science topic

I believe that you're asking two separate questions - first, will food be affected from the exposure to cosmic radiation and second what are the health issues associated with radioactive materials in food.

With respect to the first question, the effects from exposure to external radiation to food are quite low. There have been many studies performed on the effects of radio-sterilization on food (from external radiation). To make a long story short, effects were similar to that which occurred during normal food cooking. The extent isn't important here primarily because sterilization occurs at an exposure level on the order of thousands of rads - which is a lethal exposure level to humans. Therefore, while astronauts are exposed to higher radiation levels than us, they definitely aren't exposed to lethal levels.

As for radioactive materials in food, we constantly are ingesting such materials. A perfect example is radioactive K-40. About 0.017% (if I remember correctly) of potassium is radioactive potassium-40. With a few calculations, one would find that an average banana has about 900 decays per minute of K-40; I find that really interesting because we consider a lab contaminated if it has 500 decays per minute of beta-gamma isotopes over a 100 cm2 area. I could imaging that the high energy cosimic radiation could be energetic enough to cause a neutron or proton to be ejected from an atom in food (which could make that atom radioactive), but you wouldn't be able to notice a statistically valid difference in the quantity of radioactive material present before and after.

Dear Tejaswini,

Best methode to estimate fat uptake is by using Scanning Electron Microscopy (SEM).

Find attachment to know more.

It would be of some help for us to understand a bit more clearly what you want to know. Please add more details.

At our research group (SIRM), we are carrying out some projects relating health informatics and nutrition. You can search in Scholar and would then come up with older and more recent literature on the topic, see for example

Among current research areas are semantic data handling of nutritional facts on the Web, personalizing diets, and evaluating/improving the quality of nutritional (and health) information online.

BTW. You could improve the visibility of this question by adjusting the topics, e.g. including 'nutrition' and others.

Im sorry ,Idont use it

See article on folate and vitamin B-12 status in schizophrenic patients available at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3252772/#__ffn_sectitle. J Res Med Sci. 2011 March; 16(Suppl1): S437–S441

Or another article Homocysteine metabolism and B-vitamins in schizophrenic patients: low plasma folate as a possible independent risk factor for schizophrenia available at http://igitur-archive.library.uu.nl/dissertations/2006-1127-200553/c2.pdf

The reference below examines the long term effects of high protein diets on renal function and should answer your question. Although whey protein was not used in this study I cant see why there would be any additional complications with this type of protein. The main point would be to not promote levels of whey protein intake above that suggested for women or children.

Concentration of Ca or Mg in drinking water or food depend upon the type of water or food. However in drinking water the maximum permissible limit of Ca is < 75 mg/lit and Mg <30 mg/l.

Reducing food package sizes is unlikely to be effective for people who are already obese and need stronger interventions. Smart downsizing is a way to counteract the enormous supersizing that has been happening in pretty much all food categories and one that could get the support of the industry.

Instead of focusing only on nutritional improvements (which can often backfire because of misleading "health halos"), let's reduce portion sizes.

You have to look for leukemia (chronic) because apotranscobalamine is sereted by leukocyts.

Sydney, I do not see your point. We are talking here about "fraudulent titles", and you give us a remark from medical history. Remove your titles, with the exception that you are an optician. It is my recommendation to you. The other titles you use are not worth the paper they are written on... I close this subject now. Please respect this.

Resistant starches were not in my research program.

E.R.

Now you can read my article "The Role of Zinc and Copper in Autism Spectrum Disorders" (Acta Neurobiol Exp 2013; 73: 225–236) here: https://www.researchgate.net/publication/244479056_The_role_of_zinc_and_copper_in_autism_spectrum_disorders

Hello Yanick. Magnesium increases the activity of the immune system involved in the formation of antibodies and acts on cells making them more tonic, helping to protect themselves from attacks (microbes, bacteria, viruses). It also would own an antiallergic and anti-inflammatory action.

Dear Maria, did you find information about such library? Please share if you got.

According to InBody 720 manual, EDEMA index means an excessive accumulation of serous fluid in tissue spaces, which results in swelling. The normal range of this score is 0.36 ~ 0.40 and 0.31 ~ 0.35 respectly, which is maintained in a healthy person.

EDEMA = Extracellular Water / Total Body Water.

InBody720´s edema index is also used to calculate the proportion of ICF and ECF. Fluid refers to the state in which protein and mineral are mixed in Body Water and with a 2:1 proportion of ICF to ECF, the ideal range of ICF/TBF (EDEMA index 2) is between 0.31 and 0.35.

There is currently a clinical trial planned to evaluate the benefits of DHA (docosahexaenoic acid) on Traumatic Brain injury(TBI) & concussion recovery, as omega-3 fatty acids have been shown to have anti-inflammatory, anti-oxidant, and membrane-restoring effects. There are many animal studies showing the benefits of high dose DHA, as well as other omega-3 fatty acids, such as EPA in animal TBI models and some human studies. Animal studies show improvements in cognition via behavioral tasks, such as the morris water maze task, as well as increases in antioxidants like Superoxide dismutase, and improvements in the level of BDNF(brain derived neurotrophic factor), which activates secondary signaling cascades involved in enhancing synaptic plasticity, spatial learning, and neuronal signaling.

There is a nice review article that you can refer to in the Journal of Neurotrauma.

Omega-3 Fatty Acids as a putative treatment for traumatic brain injury. Hasadsri et al. Journal of Neurotrauma June 2013, Vol. 30, No. 11: 897-906

There is far more wrong with the JNCI trial than discussed, so I will here expand on your discussion in somewhat different directions, those surrounding critical appraisal. From this perspective, the findings of this trial do not achieve dispositive status, as there are divergent and contradictory findings, such as those, among others, just published from Colleen Pelser and colleagues [Pelser C, Mondul AM, Hollenbeck AR, Park Y. Dietary fat, fatty acids, and risk of prostate cancer in the NIH-AARP diet and health study. Cancer Epidemiol Biomarkers Prev 2013; 22(4):697-707] at NCI who investigated associations between dietary fats and fatty acids and risk of prostate cancer in the large NIH-American Association of Retired Persons (AARP) Diet and Health Study (n=288,268, average follow-up = 9 years, with n=23,281 prostate cancer cases, n=18,934 non-advanced and 2,930 advanced, including 725 fatal cases), finding that EPA intake was in fact related to decreased risk of fatal prostate cancer.

In addition, there are methodological issues that affect the applicability and clinical relevance of the study's conclusion, since the investigators failed to examine and thus failed to control for, the participants’ diets, and - more critically - whether participants were on omega-3 supplementation, rather common in the general population. Given the plausible possibilities that there were unexamined dietary factors of distortive influence, and that some appreciable proportion of participants were already omega-3 supplement users, a critical confounder, the conclusions drawn are reaching beyond what the data warrants and must be seen as methodologically equivocal at best. Failure of control of critical confounders was similarly exhibited in the infamous study of antioxidants and lung cancer risk (claiming to find an adverse impact, since discredited by myself and others) in which the intervention arm (antioxidant users) included smokers and investigators failed to control for active smoking: thus here, as there, we cannot with any degree of methodological equity allow for the possibility of omega-3 supplementation (or smoking, active or historic) and other possibly confounding dietary factors, and yet claim the study's power to draw the conclusions it does.

In fact, more robust and methodologically mature prospective data that control for dietary variables and, critically for omega-3 supplementation, as well as incorporating quality controls for contamination by pollutants like methyl mercury and arsenic, among others, commonly seen in marine-source proteins, and also controls for the differential effects of marine-source versus non-marine-source omega-3 fatty acids, as well as the influence of the EPA/DHA ratio rather than absolute quantities, all these and others not accounted for in the OSU (Ohio State University) JNCI trial, are required before we can support conclusions as to the true role of omega-3 fatty acids in risk of prostate cancer development in general, and advanced and/or aggressive prostate malignancy in particular.

I think the answer is dependent on how close the electronic version is the paper. We developed a web-based FFQ which totally changed the flow and presentation of the paper version and it resulted it higher accuracy during our validation study. I know of a number of studies that used an online version of a paper FFQ that for all intents and purposes was exactly the same. They used both interchangeably in their studies.

I believe lifestyle modification is the best way to remove UA from joints... If patients were with susceptiability genetics background to Gout, they should be pay more attention on lifestyle modification. This is due to susceptiability gene and environment interaction effect...

There is a research group in this area at the University of São Paulo. You could check their website and their publications. www.gac-usp.com.br

They have developed a Diet Quality Index.

Maybe it can help.

It is a very hot topic at the moment. Look at publications by Lisette de Groot, luc van Loon, Eric Ravussin, Darcy johannsen, Carla Prado, and investigators at the National Insttute on Aging at the NIH.

Food Ecology looks at contemporary human health in relation to ideal nutrition which includes not only the foods we choose to eat but how they are grown and what impact this has on the environment. Food Anthropology takes a long look at contemporary and previous cultures of human populations with respect to foods they consumed and how they were prepared. I have a personal interest in this. I focus on biochemical aspects of food preservation & preparation, human assimilation and health benefits based on ethological research.

I applied for funding for a project to increase backyard vegetable growing. The main aim was around sustainability rather than nutrition per se. Missed out on the funding but will submit it elsewhere. Anyway, this might be another angle you might pursue Mary - ie don't limit your search to nutrition as the focus. (And I'd be interested in what you uncover.)

I think we need far more information before we can answer your question.

What type of food?

What type of processing?

Regardless of the answers to the questions, the response will be very variable due to the different properties of the different vitamins and minerals, are there any in particular you're interested in?

Olá Kahlile,

eu sou aluno de doutoramento no Centro de Química da Madeira (CQM) e no laboratório de produtos naturais e química orgânica trabalhamos com plantas e alimentos, avaliamos a sua composição fenólica, medimos as respetivas atividades antioxidantes, antidiabéticas etc.

Se você estiver interessada mande mensagem privada.

Cumprimentos :)

Hi Carlos, thanks for your answer.

I know about the USDA database and in fact do use it quite often. But many foods and recipe variations are not in there.

There must be a way to test something like the pith of oranges (that white stuff right under the peel) or some of those hybrid stone fruits I always see in the grocery stores nowadays? A non-commercial (ie: not insanely expensive) lab for which such chemical tests wouldn't be too much of a hassle?

In stable patients without signs of metabolic decompesation, there is no need to reduce protein intake. In patients with hyperammoniemia or clinical signs of encephalopathy it is opportune to reduce proteins in the diet, which could been supplemented by branched chain amyno-acids.

From my present ongoing research, I can say that the the rice culture good at antidiabetic properties viz., Betasitosterol is poor or below standards for protein content. So there exists a relationship between them.

Dear Pedro Ramos to reduce glucose is not sufficient to my opinion, we must reduce calories too. Fasting has demonstrated to control tumor growth better than glucose deprivation. it is a question that my Group is studying and we think to adopt a diet with low glucose more rich in omega 3 fatty acids and with two or 3 days of calories reduction. we think also to use natural inhibitors of glucose like citric acid and thioctic acid (see metabloc)

The Paleolithic diet and the Mediterranean diet are propagated without real scientific evedence. They beared on absolutely different ideas as temporary fashions and are not well accompanied with biological or medicinal performance tests.

In contrast the ketogenic diet is a medicinal therapy as a treatment for special diseases. This diest is allowed only with medical examinations and supervision.

More information about your study design would be needed to determine the correct measure, but here are some starting points:

The 6-item short scale from USDA's Food Security Survey Module: http://www.ers.usda.gov/topics/food-nutrition-assistance/food-security-in-the-us/measurement.aspx (click on the survey tools link on the page).

direct link to pdf: http://www.ers.usda.gov/datafiles/Food_Security_in_the_United_States/Food_Security_Survey_Modules/short2012.pdf

You can turn this into a 5-question scale by modifying the answer options with two of the questions (there is a skip pattern).

In this module, there also is a "screener" option that allows for skipping the last 2-3 questions depending on the answers to the first 3 questions.

Pros and cons of various survey modules are also available through the USDA's "measurement" page and will be helpful for you to pick the right one for your study.

If food sufficiency will be an adequate measure for your study, you can find the food sufficiency screeners on the same USDA link above.

If the study will be done in a hospital setting, you may also want to check out this 2-question version published by E Hager, John Cook, Mariana Chilton and others:

Ritz BW, Aktan I, Nogusa S, Gardner EM

Energy restriction impairs natural killer cell function and increases the severity of influenza infection in young adult male C57BL/6 mice. J Nutr 2008;138:2269-75.

According to food chemistry book, some of vitamins, especially vitamin C is very sensible to heat, this vitamin degradation susceptible to small temperature Increasing.

According to the food microbiology books, some of bacteria for example Staphylococcus aureus , grow in (35-37) centigrade degree and produce poison in (10-46) centigrade degree. This poison is relatively Thermostable and don’t destroy in pasteurization temperature and can food poison.

Or Bacillus Cereus is another bacteria has risk for cooked food which is Maintenance warm for a long time (for example cooked or fry Rice). This bacterium can cause Food Poisoning.

Shod be noted, food holding in Inadequate environment (for ex holding food in dishes which has high deep ) is another risk factor, because the high temperature center of food can produce condition which is bacteria can reproduction and leading to food poisoning.

Dear Reza,

you can submit it to : Planta medica, Fitoterapia, Journal of Ethnopharmacology (for good impact factor). there are many more journals with little less IF. If you need, you can download complete SCI journal list with their respective IF's from internet @ http://www.uotechnology.edu.iq/appsciences/indexhome/promotion/Impact_Factor_2012.pdf

Good Luck..!!!

One way to improve nutritional content in the curriculum is to get it in the national requirements for medical training keeping the requirement simple so the medical schools do not feel overwhelmed and providing easy accessible material that can be used without too much effort. If nutrition is seen as a vertical strand through the curriculum along with pathology, infection. physiology and biochemistry it is more likely to be integrated throughout the curriculum rather than a stand alone issue which is learnt and forgotten.

We need clinicians to remember to consider nutrition when seeing/treating a patient rather than being a full nutritional expert. However they should know basics such as basic nutritional needs and guidelines, calculating and interpreting BMI, when to give nutritional support and be aware of the importance of using nutritional screening tools to see if referal to a dietitian is required.

Solid state fermentation with the right inoculum. You can decide to but the enzymes directly and use or you find out which organisms will provide you with the enzymes and use them.in your solid state fermentation

Nutrition is the backbone of proper cell growth and metabolism. Without it the body will not be able to sustain good health for long.

Presence of opioid like receptors viz., Bicyclo[3.3.1]nonan-9-one, 1,2,4-trimethyl-3-nitro-, (2- endo,3-exo,4-exo), triterpene squalene, alkane eicosane and antidiabetic components like ß-Sitosterol, Cholest-5-ene,3-bromo have been recently observed through GC analysis and their efficiency has to be confirmed through clinical studies.

David:

Thanks for this intriguing question.

I would note however that this data (the UCSD study from White et al. [1]) is not compelling given some methodological concerns that emerged upon my critical appraisal. Essentially what was tested was an insulin-normal model in lean young mice, but this does not in any way exclude a positive effect from muscle SIRT1 overexpression in what I would consider a far more clinically relevant insulin-resistant model; indeed, the clinical relevance and applicability - should these results ever be confirmed with true human clinical data and not just in preclinical animal studies - of absence of muscle SIRT1 overexpression is wholly unclear when observed in the absent of any significant insulin resistance. And even more critically, the UCSD White et al. results stand against several lines of contradicting evidence, as for instance the conclusion drawn in the Chinese Academy of Sciences study [2] that increased expression of SIRT1 did in fact improved insulin sensitivity, especially under insulin-resistant conditions, and with resveratrol apparently acting as a SIRT1 activator, enhancing insulin sensitivity both in vitro in a SIRT1-dependent manner and also preventing high-fat-diet-induced insulin resistance in vivo.

Furthermore, germline overexpression of SIRT1 was observed in the UCSD study (acknowledged by the investigators), in addition to large-scale (~150-fold) SIRT1 overexpression, leaving open the possibility that beneficial insulin modulation may be preempted under such specialized conditions of chronic SIRT1 overexpression and/or aberrantly large SIRT1 overexpression. White and co-authors try to counter this, implausibly, by noting that a previous Columbia University study [3] found that muscle insulin action was unaffected by two- to threefold SIRT1 overexpression from germline, but that is clearly a vastly smaller magnitude of SIRT1 overexpression (2X - 3X) from that observed in the UCSD White study, running at ~150X-fold, and no extrapolation therefore can be legitimate here.

In closing let me add that it's beyond the scope of this brief response (the last time I reviewed these issue late last year, the review ran to 85+ pages with 28 pages of references (300+) to enter authoritatively into (1) the association of SIRT1 with caloric restriction, (2) with whole-body metabolic status, and (3) whether resveratrol exerts true SIRT1 molecular activation, but I am not based on the preponderance of evidence convinced that these associations have been plausibly challenged by methodologically robust data (multiple reviews I critically appraised conclude the opposite), nor that SIRT1 activation is not observable in resveratrol operation (especially when we differentiated dose-dependent effects as per the recent Harvard/NIH study [4], among others). But that's another story. In the here and now, under critical review the UCSD study results do not materially affect the balance of evidence given unresolved methodological concerns, and the presence of a non-trivial body of contradicting data.

1. White AT, McCurdy CE, … Schenk S. Skeletal muscle-specific overexpression of SIRT1 does not enhance whole-body energy expenditure or insulin sensitivity in young mice. Diabetologia 2013 Apr 19.

2. Sun C, Zhang F, Ge X, et al. SIRT1 improves insulin sensitivity under insulin-resistant conditions by repressing PTP1B. Cell Metab 2007; 6(4):307-19.

3. Banks AS, Kon N, Knight C, et al. SirT1 gain of function increases energy efficiency and prevents diabetes in mice. Cell Metab 2008; 8(4):333-41.

4. Price NL, Gomes AP, Ling AJ, et al. SIRT1 is required for AMPK activation and the beneficial effects of resveratrol on mitochondrial function. Cell Metab 2012 May 2; 15(5):675-90.

I suggest you to use Journal Author Name Estimator website:

This is a website that analyses your text (title or abstract) and returns the journals that are most similar to your input. Very interesting.

There are too many variables relating to children's physical activity to make generalisations about which is more active. Accelerometers used in research studies have enlightened us somewhat. However, far more research is necessary to fully understand activity levels in children and why they differ dramatically in some groups.

Children that have a disability are more likely to be at greater risk as they may miss out on learning the skills necessary to remain physically active throughout life.

This is not an easy question to answer. Several plausible explanations have been hypothesized, but no one seemed to fully explain this syndrome. Aflatoxins and oxidative stress seem to play a role in addition to the malnutrition. Recently, an interesting work has been published exploring the influence of environmental factors (nutritional deficits) on fetuses that will develop marasmus or kwarshiorkor postnatal, as an adaptive response. Perhaps, these two links may help you:

I suppose it could be both. But as it appears, eventually there is a bit of hormonal basis. For example, high fat is associated with a set of alterations in endocrine balance, most common being hyperinsulinemia which is a kind of counter-regulatory measure. High levels of cortisol/corticosterone is associated with insulin resistance.

Further, i firmly believe that we really have to look at type of fuel than energy balance it self. It is exemplified by the fact that not all types of fatty acids lead to insulin resistance. Also, equal amount of glucose and fructose will have different impact.

I wont be wrong in saying that a little extra or more of starch is not dangerous as compared to same amount of sucrose or fructose.

Hi Dolors,

I'm using the Martin Moreno´s for Spanish female population. Look this page: http://www.juntadeandalucia.es/servicioandaluzdesalud/contenidos/gestioncalidad/DRECA2/E9.pdf

Regards

Hi Juan, usually consensus statements talk about 25-30% of energy intake, and never below 15%; however I know many athletes on 10% fat dieta that do very well, such as Kenyan elite distance runners. Recommendations for acyclic sports lack research, but generally these athlets like to eat 30% fat diets, although we don't know whether this is performance enhancing or not.

Conversion rate from ALA to DHA (22:6n-3) is higher in vegetarians than in omnivores, since dietary intake of LC PUFA in omnivores inhibit the delta-5 and delta-6 desaturase through a negative feedback.

Predominant n-3 PUFA in Salmon oil is EPA (20:5n-3), in Tuna oil is DHA, in Seal oil is DPA (22:5n-3) .

Heap seed oil contains about 20% ALA (18:3n-3), 60% LA (18:2n-6).

ALA, EPA, DPA and DHA have their own biological function, in this case, it is hard to say which one is more healthy. In addition, EPA, DPA and DHA can be transformed each other in humans.

Are you referring to sun deprivation in rats or humans?

To cause a depletion of vitamin D in rats is need to test various levels of dietary vitamin D(3) to achieve stable mean serum 25D levels ranging between 10 and 115 nM.

Ref:http://www.ncbi.nlm.nih.gov/pubmed/18597628#

Carbs = Sugar

Sugar in your food generally requires little to no digesting or processing and will be in your bloodstream inside 60 minutes after eating. In response, blood sugar shoots up for a bit before coming back down rapidly a short while later. Other

carbohydrates, referred to as complex carbohydrates, will be sugar in your bloodstream as well eventually. It takes your digestive system a little longer to convert complex carbs into simple sugars, so blood sugar will rise and fall a bit slower depending on a few factors. These include

the type of carbohydrate (how "complex" it is) and how fibrous and/or fatty the food is.

Once in the blood, your metabolism begins to use sugar in a variety of ways. Particularly if you are active or exercising, some of the sugar in your blood will be

used quickly for energy. Glucose and/or fructose are the end-products of all carbohydrate breakdown. These simple sugars enter into either glycolysis (for glucose) or fructolysis (for fructose). In these processes, the metabolism uses the simple sugars to generate the compounds

that, in turn, power all of the body's other metabolic processes. Put more simply, glycolysis and fructolysis convert simple sugars into energy.

(A quick note on fiber: fiber is classified as a type of carbohydrate and is listed on nutrition labels under the

carbohydrate section. Most fiber will pass through the body undigested. The remainder will be digested quite slowly over the course of many hours. Fiber does not have a meaningful effect on blood sugar.)

Insulin: The Storage Hormone

Most of the time, however, sugar is not used immediately but is stored in cells for use later. This is where insulin comes into the equation. Insulin is a protein that acts as a hormone in the digestive process. When a protein is classified as a hormone, it means that it's

presence in the bloodstream triggers a cascade of other related and interdependent processes in the metabolism. Insulin is perhaps the single most important element of nutrient metabolism, and understanding its function is critical for understanding what your body is doing with the food you eat. When

there is more sugar in the bloodstream than the body is immediately using, insulin is released and initiates the storage process. Insulin causes glucose to be absorbed into cells, upon which, it is stored in one of two ways. The primary storage method for glucose is as triglycerides in adipose

(fatty) tissue. The secondary method is as glycogen, essentially a matrix of glucose that is stored in muscle and liver cells for later use as quick energy, primarily in times of exertion.

To summarize, when you eat carbs they are broken down

into sugars by the digestion process. Sugar causes the release of insulin and insulin causes the sugar to be stored, primarily as fat in adipose cells. Particularly when forming a large portion of your caloric intake, carbohydrates are the primary source of any fat your body is storing.

Fueling With Fats

Fat digestion and metabolism happen via completely different pathways than the ones used for carbohydrate metabolism. The first major difference in the digestion of fats relative to

carbohydrates is that the breakdown and absorption is a much slower process. Most fats are broken down slowly in the gut via a series of enzymes called lipases and eventually make their way into the blood stream as free fatty acids. Like sugars, once in the bloodstream free fatty acids can be used for

energy (via the process known as ketogenesis) or stored in adipose (fatty) tissue for later use.

One notable exception to this digestion pathway is medium-chain triglycerides (MCT's). Because they are smaller than other fats, MCT's can pass directly into

the bloodstream without needing digestion in the gut by lipases. These smaller fats are broken down into free fatty acids by lipases in the blood rather than in the gut. While other types of fat take too long to digest and process to be a legitimate alternative to carbohydrate as a primary fuel source, the

quicker availability of MCT's makes them not only a legitimate alternative, but a preferable one. MCT's are also unique among fats in that they can be used by the brain for energy. Other types of fat must go through the long process of being converted into sugars before they can be used by the

brain. Eating primarily other types of fats would leave the brain under-fueled. Once again, MCT's and SCT's not only solve this issue, but offer a superior alternative to carbohydrate. Unsurprisingly, MCT's and SCT's are critical to any diet using fats as a the primary calorie and fuel source.

When your metabolism is using primarily fats as an energy source, you are essentially "training" your metabolism to use fats more often and more efficiently. The metabolic pathways involved in ketogenesis (fat-burning) become more robust, and the body

becomes better at using fat stored in adipose tissue when available sufficient calories are not available from food intake. Fats also don't directly trigger an insulin response, so the body doesn't go into "storage mode" as often when fats are your primary fuel source.

So what are the best sources of MCT's? Coconut oil (and related products) and grass-fed butter are hands-down the top choices. Coconut oil is about 2/3 MCT's by weight. In addition to it's many other benefits coconut oil is the go-to fuel source for many people adhering to this type of high-fat diet. A

few companies isolate the MCT's from coconut oil and sell "MCT oil" by itself. This is a pricy option as an every-day fuel source, but if you're looking to accelerate the fat-burning capacity of a this diet, MCT oil is a powerful tool. Coconut butter is also a great choice, as it is the "meat" of the coconut before

the protein and fiber is pulled out in the process of making coconut oil.

Additionally, grass-fed butter is an excellent source of short-chain fatty acids (as well as many vitamins and Omega-3 fatty acids). These short-chain fatty acids behave in much the same

way as MCT's and can be used for the same purposes. It is important to source only 100% grass-fed (sometimes called "pastured") butter. Conventional butter has a significantly different nutritional profile and is more likely to contain toxins.

Fats vs. Carbs

the metabolism tends to adapt to the types of fuel it is receiving most frequently. If the metabolism is being fueled disproportionately with carbohydrates, the metabolic pathways that use and store carbohydrates will dominate while fat metabolism pathways will

diminish. The reason for this is two-fold. The first reason is that the pathways required to store or use carbohydrates require a set of enzymes unique from those the metabolism uses to process fat. The body is remarkably good at not being wasteful and will decrease production of fat

metabolism enzymes when they are used infrequently. The second reason is that insulin specifically stops the use of fat for energy by inhibiting the release of glucagon, a hormone that increases blood sugar and thus directly competes with insulin.

Because of this "competition" between fat and carbohydrate metabolism pathways, fat will only be used for energy in the absence of insulin. If you're going to train your body to use fat for energy, it becomes critical to minimize both the magnitude and duration of any spike in

blood sugar and thus, the magnitude and duration of the corresponding insulin release.

Glycemic Load, Glycemic Load, Glycemic Load

If you're aiming to minimize insulin response and support your body's fat-

burning metabolism - there is one concept that stands above all the rest to use when judging the effect of a given food. That concept is, of course, glycemic load. Glycemic load is essentially a measure of how much a given amount of a certain food will increase blood glucose levels after eating.

With the exception of a few specific situations (nutrition during an intense workout is one such exception), you should focus on keeping the glycemic load of any meal relatively low. Keeping the glycemic load low will minimize the amount of insulin released during and after eating. This will in turn

minimize both the amount of carbohydrate from your meal that is stored as fat - and - minimize the time in which fat-burning metabolism is suppressed.

Yes, it should be. In fact mineral oil (Duoprime oil 90) contains white mineral oil and alpha tocopherol (Vitamin E) as ingredients.

Alpha tocopherol is soluble in fat. So just take a small quantity and clear your query.

The question was to discuss or give advice for methods analysing B-vitamins in plasma. For B1 (thiamine) there are many HPLC methods with fluorescence detection of the thiochrome derivatives of thiamine and its phosphates; we analysed thiamine, TMP and TDP in whole blood and breast milk using this method (see Stuetz W et. al 2012). TDP (thiamine diphosphate) is the main thiamine compound you can find or detect in erythrocytes and therefore also in whole blood, while only small amounts of thiamine, TMP and TDP will be found in serum or plasma; the question remains if plasma is a good indictor for thiamine status.

Vitamin B2 (Riboflavin, FMN, FAD) can be directly detected by HPLC and fluorescence, and here (similar to TDP in thiamine analysis) probably FAD is the best indicator for riboflavin status; I'm not sure if it make sense to analyse in plasma or serum ( we are on the way to analyse FAD, FMN, and riboflavin in both serum and erythrocytes).

For folate analysis you will find high levels of 5-methyl tetrahydrofolate in erythrocytes and whole blood; this can be measured by HPLC and fluorescence after incubation of the blood samples for some hours in ascorbic acid solution (plasma carboxylase at a pH of 4.5 will release the many polyglutamatic folate forms). Again in plasma you will find only small amounts of 5-M THF and this could be analysed by MS.

There are methods using ELISA for B12 and folate in plasma. But you could also analyse these B-vitamins by HPLC-MS.

Hi,

Concerning the NPRQ, i don't know other equations than the classical VCO2/VO2.

Then, concerning substrate oxidation, to my knowledge, the equations are the following ones.

Carbohydrates (mg/min) = 4.58R VCO2 - 3.2255 VO2

Lipid oxidation (mg/min) = -1.7012 VCO2 + 1.6946 VO2.

If you need more informations, you should have a look on articles from Brun JF et al. He worked on substrate oxidation during exercise.

Hope this helps

Its the Great Area to work with, but the space is occupied by Pharmaceutical Comp. Formulating supplements for health is vast space. Formulating nutrition to augment Health outcome is still Naive in India. I would be interested to collaborate with such team

Dear Thomas,

It is not about the collaboration of "all" nutritionists. It is about being open to collaborations and looking forward to it. Being just straight minded about one field is against the interdisiplinarity which brings innovation and creativity into the field and I am telling it as both a nutritionist and food scientists.

No doubt that humans lived with out food industry for a long period, but we are not talking about cave mans anymore. Life styles changed, human behaviors changed, and so as the physiological concepts of human body. So if persons involved with food, do not collaborate, the future path will not be so clear or even promising.

What I am trying to imply here is the lack of trust and openness between the researchers of these fields. To be honest, I even feel anger in your sentences. Anger for food science and that is the draw back which many nutritionists have.

I agree that there are conflicts in the industry due to many reasons, but nutritionists are a part of food chain too. They need to play their roles. Industry has fund and resources, nutrition has well designed research. Who can say that a true and healthy collaboration will do harm?

I really hope that we get to a conclusion of seeing more friendship in these two fields.

Regards.

Speaking as an Optometrist with 55 yrs experience of studying the health of the retinal microvasculature and the Optic Nerve; having just written the foreword to a new book about to be published "Nutrition for Optometrists and You;" and having recently published "700 Vitamin C Secrets, and 1,000 Not So Secret For Doctors;" teasing the medical profession about Pharmacy's restrictions on medical schools curricula, I would like to answer this question. The answer every nutritionist would give is "We are what we eat!" One's immune system is a complex combination of endocrinal, hormonal, lymphocyte blastogenesis, antioxidants, antibodies, cytokines, immunoglobulins and more that I am totally unqualified to write about! So why do I betray my lack of in depth knowledge? Because after considering the importance of all these factors and doubtless more to be discovered, the most important single factor appears increasingly to be that identified by Linus Pauling - Vitamin C. Not even a vitamin in reality but a vitamin-like multitasking substance with profound importance as neurotransmitter, foundation of hormones, creator of collagen (our most important protein) origin of the hypochlorous acid that is basic to phagocytosis, protector of the cytoplasm and mitochondria of the white cells, protector of the retina against UVB converting UVA into the longer wavelength radiation, and generally so basic to our immune systems that without it we would have no immune system. Now to answer the question having laid the foundation we can consider the need for supplements. Before supplements and farming, Man could find nothing to eat that would not put vitamin C on his tongue. The purist will suggest honey and bee propolis? Yes. They are the only exceptions assuming we do not eat old bones or the dead animals we are admonished in the Bible not to consume. The need for ascorbate supplement has been created by modern diets of Man who is unlike the animals that can make it in their liver (goats up to 100,000mgs/day) or cold blooded animals more in their kidneys. The meat eating Masai and Inuit, appear to get enough from their diets but the weaker individuals may have been bred out. There are also pronounced gender and age related variations in the amount of ascorbate we need. Interestingly, we need an exponentially increasing amount particularly with ageing. Russell Jaffe showed that some can need up to 130,000mgs/day to maintain their immune systems as I've said before here. CardioRetinometry has shown that the RDA for vitamin C is literally, fatally flawed, one child having been found to need 1,000mgs/day for a healthy heart. The RDA has led to the current pandemic of coronary thrombosis, stroke, angina etc. That the USA RDA is four times the UK RDA appears indefensible. Until people understand that medicine, adequately warned by the Sardi Expert Committee on Aug 24th 2004,, as described in the Hickey & Roberts RDA book, prevents upgrading of the RDA, the official position is that the NIH deliberately maintains cardiovascular disease for profit, criminally aided and abetted by our UK institutions. That is now irrefutable. Prof. Denham Harman and Dr Frederick Klenner were both fully entitled to Nobel Prizes but were denied them because it would have brought too much attention to vitamin C, scurvy being the origin of over 50 profitable diseases.

I am utilizing Transitions Theory as the framework for my dissertation related to outcomes after lung transplantation. I have been through the literature pretty thoroughly and do not recall any citations for this particular topic. I know that there is no mention of this type of transition in Meleis's book. (Transitions Theory: Middle range and situation specific theories in nursing research and practice).

I did find this citation below. I don't have access to full text for this article to tell if transitions theory is utilized as a framework. It might be worth a look, though.

Shannon Reedy and Kay Blum. Bariatric Nursing and Surgical Patient Care. March 2010, 5(1): 35-43. doi:10.1089/bar.2009.9940.

Hi Anna

Please try with this document

Institute of Medicine. Food and Nutrition Board. Dietary reference intakes for vitamin A, vitamin K, arsenic, boron, chromium, copper, iodine, iron, manganeze, molybdenum, nickel, silicon, vanadium, and zinc. Washington, DC: National Academy Press.

Are you aware that a software already exists? Maybe that's saving you of a lot of work. See www.dietcheckmunich.de

semicabazide is the same than semicarbazine (it is an error), Semicarbazine is the free base, and the other is the chloride salt. The free base is not stable around 100ºC. At solution, the pH determines which form is predominant.

I agree with Lluis, you have to be audience specific. Things could differ based on food handler's race, gender, age, geographic location, etc etc (there could be more modifying variables)

The muscle mass increase was shown first by Geoff Goldspink. You should check for others, but I think that the key references are:

Goldspink, G. (1985). "Malleability of the motor system: a comparative approach." Journal of Experimental Biology 115: 375-391.

Goldspink, G., A. Scutt, et al. (1991). "Stretch and Force Generation Induce Rapid Hypertrophy and Myosin Isoform Gene Switching in Adult Skeletal Muscle." Biochem Soc Trans 19(2): 368-373.

Increased sarcomere counts are in:

Lynn, R. and D. L. Morgan (1994). "Decline running produces more sarcomeres in rat vastus intermedius muscle fibres than incline running." Journal of Applied Physiology 77(5): 1439-1444.

The protection against injury has lots of papers back to the 1980s.

(Armstrong et al., 1983; Newham et al., 1983; McCully and Faulkner, 1985).

My favourite experiment for the importance of long length is walking down stairs two at a time in:

Morgan, D. L. and U. Proske (2004). "Popping sarcomere hypothesis explains stretch-induced muscle damage." Clinical and Experimental Pharmacology and Physiology 31(8): 541-545.

That will also have references for others.

If Zinc deficiency has any relevance to endothelial function, exclusion and inclusion studies will quickly reveal it by CardioRetinometry. (Google for it - PubMed will tell you nothing)

This is a huge question. In general, from the medical point of view, such studies never give definite answers and are only the first step. The effectiveness of a tested compound in vitro or in animal models is not a prove that it works the same way in human or, IF it works in the same way, that such activity is of clinical importance. The typical example is resveratrol from grapes - most studies made in animals or in vitro, lots of them very promising, but in clinical trials the effectiveness restricted and data confusing.

On the other hand resveratrol is a good example of the above mentioned multi-step strategy. Just a few days ago Seidman et al. showed that resveratrol decreases noise-Induced cyclooxygenase-2 expression in the rat cochlea. COX-2 levels are induced following noise exposure so showing the effectiveness of resveratrol in rats may open the way for future studies in humans that are at risk of noise-induced hearing loss.

Of course we have to remember that bioactive compounds from foods interact and the final influence of several foods does not reflect the sum of their bioactive compounds but also internal (and external) interactions. Anti-oxidative compounds (for example resveratrol) are good example here, because in cell they act as cascades.

The key here is to be evidence based. The human physiology is designed to digest both animal and plant foods. You only need to consider dentition and bile acids and also the human range of required essential nutrients which our bodies cannot make. Adequate amount s of the later are best achieved through a variety of foods from both animal and plant sources. However, with modern opprotunities it is easier to obtain nutrients but also easier to overeat with less requirements for energy expenditure.

We need to have moderation but variety, plant food in the diet should certainly outnumber meat intake but this is also the basis of most dietary recomendations.

Looking back to paleolithic diets does not really help. Life expectancy should also be taken into acoount. When we learned to cook we imporved our nutrition. In more recent times we have growth taller, live longer and due to good nutrition and other medical and sanitation devepments on the whole has better health and quality of life.

To say if meat was safe in the past, it must be safe now does not allow for the changes in the meat and meat products that we eat. There is a considerable evidence base for red and processed meats to increase colon cancer risk (WCRF 2007). The key is moderation and dose effects.

The company I am working (Buhler) has developed a technology which enriches rice kernels with iron. You can then mix the enriched kernels with normal rice. Look under www.buhlergroup.com for more information.

Mary Huber: in your own words, "Protein deficiency is common among vegetarians and vegans for obvious reasons". This is a statement which is totally inaccurate and demonstrates not only your complete ignorance of clinical nutrition, but your propensity to state things as factual which you have somehow decided must be true, though in fact have no place in reality. Since, based on true statistics (from the real world), protein deficiency is far more common amongst meat-eaters than vegans or vegetarians, how in the name of anything holy could you make a statement that protein deficiency is far more common among vegetarians and vegans? Might I suggest that you do a little scientific research and check the facts (from the real world) before stating lies as scientifically?

I believe, 8 - 11 years age group is mature in the present century , to be able to be attracted towards celebrity endorsed products and would be gender conscious too! Although, as pointed out, older age groups will be more influenced and it would be an interesting study !

This is the most hilarious forum I've ever joined. Nobody has ever proved a link even between CHD and moderately 'high' cholesterol or of protection from a moderately 'low' cholesterol. Statins have been said to be "better in secondary than primary protection". (You've got to HAVE a first heart attack before you might get a benefit preventing a second!) The many studies that have been done have cooked the results to save red faces. The fifty years of trying to prove a link have proved there is no link. The investment in statins to prove a benefit has backfired and proved the reverse. Ravnskov's seminal work is being pointedly ignored. Everyone should read his "The Cholesterol Myth, Exposing the Fallacy that Saturated fat and Cholesterol Cause Heart Disease." Corruption is exposed on pages 40, 58, 69, 78, and 131, He shows how Ancel Keys' original paper was wrong to the point of being fraudulent - omitting the figures for France and Mexico that completely refuted his hypothesis. How - as Ravnskov asks - does one explain the "French Paradox" or the fact that of the apparently identical Greeks living on Corfu and Crete, Those unlucky enough to live on Corfu have five time more CHD than those on Crete? The Mediterranean diet is confounded! How does one explain the difference between E and West Finland? How does one explain the highest possible sat fat Masai diet winning Marathons? How does one explain my father nearly dying twice in his 40s and me - his double - having no coronary disease at going on 85 living on Atkins diet -of zero carbs and 4 pints of full fat best organic milk / day - no arthritis etc just a blown mitral valve - my own silly fault for leaping up the stairs two at a time five stones (250lbs/110Kg) overweight at age 80 and only just 5' 8" ? Give me a good healthy diet of saturated fat that my body makes (it doesn't make rapeseed oil) and lots of cholesterol. I love it. Best - Sydney.

PS

If You are really worried you'll send me your arteries in a fundus photo for evaluation - I've never charged a colleague. (Send to ProfBush@InstituteOfCardioRetinometry.ac) Don't believe what you are taught - that the fundus arteriolar reflex is a "Healthy Sign" - it a very UNHEALTHY sign for you are looking directly at intraluminal plaque which in many cases is continuous with the Hollenhorst Microplaque. At the Anti-Ageing Conference I shall prove that the reflex cannot come from the blood column as advanced by Brinchmann-Hansen. How on earth we could have fallen for that rubbish for so long I can't understand. But I was just as stupid as the rest. We all fell for for it. Szent-Gyorgyi said DISCOVERY is "See what everybody has seen, and thinking what nobody has thought." Now we make the plaque dissolve away and watch it go.

www.LifeExtensionOptometry.org shows how.

The high carbohydrate and fatty diet is the cause for both Diabetes and obesity. As carbohydrate rich food in the diet causes excess release of the insulin in initial stages in a period of time it leads to insulin insufficiency. Where as high fat content diet causes hyperlipidemia and obesity and also fatty liver , as liver also regulates blood glucose. So, both should be taken less. Fiber rich food with good amount of protein is beneficial.

The risk of bias due to inappropriate randomization in a crossover trial design is not as large as in a parallel arm design, because individuals act as their own controls. As long as the treatments do not have a potential carry-over effect, due to a insufficient wash out period between phases. When doing a systematic review there are scoring systems that can be used to measure overall quality of the trials that meet the rest of the review criteria. A threshold quality score can then be used as an additional inclusion criteria for the review. These scoring systems typically give more value to appropriately randomized and controlled trials.

Dear Dr. Kurhekar,

According to me BMI and BMR are very important measure of human health. BMI is a useful measure of overweight and obesity. The higher your BMI, the higher your risk for certain diseases such as heart disease, high blood pressure, type 2 diabetes, gallstones, breathing problems, and certain cancers.

Regards

Ioannis Patrikios

There are eight naturally-occurring isomers of Vitamin E, that is, alpha- , beta- , gamma- and delta-tocopherols and alpha- , beta- , gamma- and delta-tocotrienols.

Gamma-tocopherol is only one form of Vitamin E, and incidentally a very powerful one in the defence against disease.

Unfortunately most Vitamin E supplements only provide us with a one or two isomers of this vitamin, doing away with the myriad of antioxidant benefits that the other isomers offer in their own particular way.

Hoping this helps.

II believe so...Please write to my email michael.gonzalez5@upr.edu

Hi dear jagdish

the beter review is the metaanalysis review.

... These data suggest that there is a reserve capacity built into signalling pathways. This raises the question "is this reserve capacity important and physiologically relevant?"

MY ANSWER: Signalling pathways are enzyme pathways and enzymes are essentially never active at their Vmax; rather, they are active at around their Km, so that small changes in substrate concentration result in significant changes in the rate of product formation and so metabolism is finely tuned.

Similarly, the hearth has a performance reserve of 400%, the brain's is even higher. The reserve capacity is the basis of adaptation of the cell or the organism to the changing environment. No reserve, no adaptation, no survival (no surprise).

Hi Geir

This is an intresting TOPIC.

I do think yes,many factors are contributing to make people sicker such as:chang in attitude,people in 1900 were more kindness,more calm and at least competition for earn money and power than today's people.These lend today's people to stress. Here is a link to "Psychological Stress and the Human Immune System: A Meta Analytic Study of 30 Years of Inquiry" in Psychological Bulletin (2004), July, 130(4), 601-630. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1361287/ .

Finaly ,in my opinion,today's people must be respect to this attitude .

I know that Venezuela has built citizen centres for elderly, which include provision of lunch, as well as a medical clinic, and recreational activities. They may have been evaluated as part of the WHO evaluation of the 'barrio adentro' programme - a good person to ask would be Carles Muntaner at University of Toronto - he did the evaluation, and may know what other research is being/has been done.

As a researcher I am also an educator in EBM (evidence-based medicine), including both eb-CAM (evidence-based CAM) and eb-IM (evidence-based integrative medicine), so I will provide here first the five most authoritative official definitions of CAM (complementary and alternative medicine) in current use, and offer some brief commentary, then finally offer a Working Definition of CAM based on a distillation of the best of these definitions and from decades of professional experience.

There are currently five authoritative definitions of CAM in widespread use:

NCCAM (National Center for Complementary and Alternative Medicine)

“Complementary and alternative medicine is a group of diverse medical and health care systems, practices, and products that are not presently considered to be part of conventional medicine; that is, medicine as practiced by holders of MD (medical doctor) or DO (doctor of osteopathy) degrees and their allied health professionals, such as physical therapists, psychologists, and registered nurses.” [1]

The Cochrane Collaboration (Cochrane)

“A broad domain of healing resources that encompasses all health systems, modalities and practices and their accompanying theories and beliefs, other than those intrinsic to the politically dominant health systems of a particular society or culture in a given historical period.” [2] Note that the Cochrane Definition has been adopted by the CAMDoc Alliance, constituted by The European Committee for Homeopathy (ECH), the European Council of Doctors for Plurality in Medicine (ECPM), the International Council of Medical Acupuncture and Related Techniques (ICMART) and the International Federation of Anthroposophic Medical Associations (IVAA), now representing 132 European associations of medical doctors actively practicing CAM.[7] See also their Model Guidelines for the Practice of Complementary Therapies (CAM) by Medical Doctors in the European Union [8].

British Medical Association (BMA)

“Those forms of treatment which are not widely used by the conventional healthcare professions, and the skills of which are not taught as part of the undergraduate curriculum of conventional medical and paramedical healthcare courses.” [3]

CAMbrella

CAMbrella is a pan-European research project on CAM that has completed a comprehensive study of the nature and definition of CAM, and has just (2012) published its definition:

"Complementary and Alternative Medicine (CAM) utilised by European citizens represents a variety of different medical systems and therapies based on the knowledge, skills and practices derived from theories, philosophies and experiences used to maintain and improve health, as well as to prevent, diagnose, relieve or treat physical and mental illnesses. CAM has been mainly used outside conventional health care, but in some countries certain treatments are being adopted or adapted by conventional health care." [4]

CAM-Expert Definition / Zollman/Vickers

From acknowledged CAM experts Catherine Zollman and Andrew Vickers, Research Council for Complementary Medicine, London, and now (Vickers) with Memorial Sloan-Kettering:

‘Complementary and alternative medicine (CAM) is a broad domain of healing resources that encompasses all health systems, modalities and practices and their accompanying theories and beliefs, other than those intrinsic to the politically dominant health system of a particular society or culture in a given historical period. CAM includes all such practices and ideas self-defined by their users as preventing or treating illness or promoting health and well-being. Boundaries within CAM and between the CAM domain and that of the dominant system are not always sharp or fixed." [5]

Commentary:

1. In general, complementary medicine refers to therapies used in combination with conventional medicine, while alternative medicine is used in place of conventional medicine, but what constitutes alternative or complementary when seen from a conventional medicine perspective may be, or become, traditional or mainstream for some ethno-cultural groups and/or at various points in history: thus use of Traditional Chinese Medicine (TCM) by the Chinese community within which it is conventional not alternative.

2. It should also be noted that the complementary versus alternative subcategories are contextual, not absolute: thus acupuncture therapy is complementary in one context as for analgesia w/wo traditional analgesics, but is alternative in another, where acupuncture is used instead of physiotherapy for muscular pain.

3. In addition, boundaries within CAM, and borders between the CAM domain and that of conventional medicine, are neither consistently clear nor constant, and these boundaries and borders change and are shaped over time across a continuum of gradually increasing acceptance and integration with conventional medicine.

4. The BMA definition is an especially poor one in claiming that CAM skills "are not taught as part of the undergraduate curriculum of conventional medical and paramedical healthcare courses." Even as of a 1989 survey [6], 64% of USA medical schools surveyed offered 1 or more courses in CAM, or these topics were covered in required courses, and 37% of the medical schools surveyed offered 2 or more courses. Since 1989, both the number of medical schools, and the number of courses on CAM within those schools, has increased dramatically.

5. Nonetheless both significant resistance and sometimes manifest hostility to, as well as ignorance about, CAM remains even today.

So based on experience and research, I will offer the following more constructive definition of CAM that has served well in instruction and in professional interaction:

WORKING DEFINITION OF CAM

An umbrella term for a collection of diverse approaches outside of the narrower framework of conventional medicine for the maintenance and improvement of health, for disease prevention and treatment, and for various associated supportive functions. In addition, when CAM is subject, as it must be, to the same methodological rigors of review and appraisal as any evaluable conventional modality using the protocols and constructs of EBM (evidence-based medicine), we term that eb-CAM (evidence-based CAM). Furthermore when CAM is integrated with conventional medicine, we term that Integrative Medicine and when that in turn is subject to EBM constraints and requirements, we term that eb-IM (evidence-based Integrative Medicine).

Forward Statement:

In systematic reviews and critical appraisals of CAM and its sister disciplines, eb-CAM, IM, and eb-IM, the weight of the evidence supports a finding of "probable efficacy" (Level I and Level II) for dozens of CAM modalities, supported by systematic review, meta-analysis, and critical appraisals, at the level of RCT (randomized controlled trial) [as, with melatonin, ginger, acupuncture, and numerous others evidenced within eb-CAM], and of course the judgment of only "possible efficacy" or "lack of (demonstrable) efficacy" for many more. As CAM, especially eb-CA matures, it is to be expected that significant bodies of CAM modalities, interventions and agents will be winnowed out by critical appraisal and failure in human clinical RCTs, but that nonetheless a significant albeit smaller body will achieve probably efficacy and be ultimately integrated into conventional medicine, a progress we are already beginning to witness.

References

1. National Center for Complementary and Alternative Medicine (NCCAM). The Use of Complementary and Alternative Medicine in the United States. Available at http://nccam.nih.gov/news/camsurvey_fs1.

2. Wieland LS, Manheimer E, Berman BM. Development and classification of an operational definition of complementary and alternative medicine for the Cochrane collaboration. Altern Ther Health Med 2011 Mar-Apr; 17(2):50-9.

3. British Medical Association (BMA). Complementary Medicine—New Approaches to Good Practice. Available at http://www.bma.org.uk/ap.nsf/content/publicpetitioncam.

4. Falkenberg T, Lewith G, di Sarsina PR, et al. Towards a Pan-European Definition of Complementary and Alternative Medicine – a Realistic Ambition?. Forsch Komplementmed 2012;19(suppl 2):6–8.

5. Zollman C, Vickers A. What is complementary medicine? Br Med J 1999; 319: 693–696.

6. Wetzel MS, Eisenberg DM, Kaptchuk TJ. Courses involving complementary and alternative medicine at US medical schools. JAMA 1998 Sep 2; 280(9):784-7.

7. CAMDoc. The CAMDoc Alliance. Available at: http://www.camdoc.eu/index.html.

8. CAMDoc. The CAMDoc Alliance. Model Guidelines for the Practice of Complementary Therapies (CAM) by Medical Doctors in the European Union. Available at: http://www.camdoc.eu/Pdf/Model%20Guidelines%20CAM%20Practice.pdf.

Constantine Kaniklidis

Director of Medical Research,

No Surrender Breast Cancer Foundation (NSBCF)

European Association for Cancer Research (EACR)

From my own recently completed internal review (commissioned for a evidence-based New Zealand guidelines authority), the systematically reviewed and critically appraised evidence to date support the conclusion from multiple Class II RCTs ("probably effective" level) [2,3,4,7,8], cross-confirmed by Level I systematic reviews or meta-analyses [11-14], of the probable efficacy of magnesium in the prevention and clinical therapeutic management of migraine disorder, in agreement with recommendations to same effect from the latest just released (2013) AAN (American Academy of Neurology) and AHS (American Headache Society) Guidelines [1], in further agreement with Canadian and several other evidence-based guidelines and consensus statements, and without clinically relevant risk of harm and with manageable adverse events (diarrhea).

The AAN/AHS Guideline of NSAIDs and Other Complementary Treatments for Episodic Migraine Prevention in Adults (2013 Update) [1] reviewed 284 abstracts from which 49 Class I or Class II studies on migraine prevention were extracted, with a subset of 15 studies using nontraditional therapies, NSAIDs, or CAM (Complimentary and Alternative Medicine) interventions. Magnesium was originally (2000 Guideline) found to be probably effective for migraine prevention on the basis of 2 positive Class II (double-blind, placebo-controlled trials) studies [2,3], weighed against one negative Class III study [4] in which intravenous magnesium was effective as an abortive agent in patients with low ionized magnesium levels, but not in those with normal magnesium levels. I note here that the fact of the weight of the evidentiary support being for probably efficacy (Level II) should be placed in the wider context that the only natural agent with Level I ("effective") evidence of benefit in migraine is butterbur (standardized on petasin content).

Post the 2000 AAN/AHS Guideline, we also have the additional evidence of efficacy from the RMF (Riboflavin, Magnesium, Feverfew) RCT [5], a Class II trial, which evaluated the combination of magnesium (300 mg), riboflavin (400 mg), and the CO2 feverfew extract extract, MIG-99 (100 mg), against placebo (subtherapeutic dose of riboflavin (25 mg)), but this trial's positive findings are restricted only to the RMF combination and underpowered to determinate relative individual component efficacy, and so this study although cited in the AAN/AHS Guideline (2013) failed to meet the inclusion criteria of my review.

The first eligible prospective, multi-center RCT [2] was a therapeutic, not preventive, 12-week trial of magnesium citrate 600 mg versus placebo which found a significantly higher reduction in episode frequency in the final month of treatment relative to baseline in the intervention (magnesium) arm compared to the placebo group. We note in this connection that magnesium is the only preventive agent, traditional or alternative, to hold a Category-A pregnancy rating, making it an feasible choice for prophylaxis in women who are pregnant or actively attempting conception, with a recommendation of maximal dosing at 350 mg/daily in pregnant women suffering migraine (Health Canada [6]). And the RCT of magnesium prophylaxis for menstrual migraine [3] found an associated reduction of headache days for the magnesium (360 mg/d) intervention, and the examination of intracellular Mg++ levels suggested that magnesium deficiency may induce a lower migraine threshold.

In another recently (2012) reported clinical trial [7], 133 migrainous patients were randomly assigned into three intervention groups: M (magnesium oxide, 500 mg/day), C (l-carnitine, (500 mg/day), and MC (magnesium plus l-carnitine (500 mg/day each), and a control group, for 12 weeks, with magnesium supplementation showing manifest and significant reduction in all migraine indicators.

We also have the São Paulo University double-blind RCT of intravenous magnesium sulphate (1000 mg) [8] that concluded that IV magnesium was effective for the treatment of all symptoms in migraine with aura, as well as an adjuvant therapy for associated symptoms in patients with migraine without aura.

And although another RCT [9] failed to unequivocally demonstrate the superiority of oral magnesium oxide over placebo in preventing frequent migrainous headache in children, it nonetheless did lead to a significant reduction in headache days.

And although the Turkish RCT [10] of magnesium prophylaxis in non-aura migraine is often cited as a positive trial, it failed to meet my inclusion criteria due to serious methodological compromise due to highly unequal sized treatment groups (total n=40, but placebo group with only 10 patients).

As to systematic reviews, one recent German review [11] conducted a comparison of double-blind RCTs on the efficacy of propranolol, topimirate, feverfew, butterbur, riboflavin and magnesium, showing that natural preparations had comparable efficacy to the pharmaceuticals but with fewer adverse effects.

In another review of non-pharmacological interventions for migraine prophylaxis [12], it was concluded that "The prophylactic efficacy of magnesium, particularly for children and menstrually related migraine, has recently been substantiated".

In addition, the CHS (Canadian Headache Society) Prophylactic Guidelines Development Group Systematic Review of Medications for Migraine Prophylaxis [13] concluded with respect to magnesium: "We recommend that clinicians offer magnesium to eligible patients for migraine prophylaxis. There is some evidence for benefit and side effects are minimal. Due to the contrary evidence presented in these trials, we recommend that 24 mmol (600 mg) of elemental magnesium daily as magnesium citrate be used for migraine prophylaxis, since a positive result was only obtained with this compound".

Furthermore, the CCF (Cleveland Clinic Foundation) Review [14] concluded that the data extracted suggests that magnesium may be effective in treating all symptoms in patients experiencing migraine with aura across all migraine patients.

Finally, as the negative AEs or interactions: (1) one RCT [15] cautions that the addition of magnesium to another not uncommon migraine intervention, metoclopramide (Reglan), may negatively attenuate the effectiveness of metoclopramide in relieving migraine, likely but not decisively from countertherapeutic cerebral vasodilatation caused by magnesium; (2) in migraine-therapeutic range (~300 - 600 mg/daily), the principle adverse event of diarrhea remains mild to moderate in most users and manageable (one field trick is to consume the divided magnesium doses concurrent with daily calcium, since most supplement with 1500 mg calcium/daily for bone health (in divided dosing of 500 mg) which appears to help counteract the side effect).

As to plausible etiology related to magnesium, it will be more appropriate to discuss this in a separate posting (forthcoming), a complex and emerging - and fascinating I might add - understanding beginning to take shape with recent pathopysiological, molecular and genetic data, all furthermore with subtle intersections with copper, melatonin and CoQ10 metabolic activities, and magnesium at the spider-center of it all.

References

1. Holland S, Silberstein SD, Freitag F, Dodick DW, Argoff C, Ashman E, Quality Standards Subcommittee of the American Academy of Neurology and the American Headache Society. Evidence-based guideline update: NSAIDs and other complementary treatments for episodic migraine prevention in adults: Report of the Quality Standards Subcommittee of the American Academy of Neurology and the American Headache Society. Neurology 2013 Feb 26; 80(9):868-9.

2. Peikert A, Wilimzig C, Köhne-Volland R. Prophylaxis of migraine with oral magnesium: results from a prospective, multi-center, placebo-controlled and double-blind randomized study. Cephalalgia. 1996;16(4):257–263.

3. Facchinetti F, Sances G, Borella P, Genazzani AR, Nappi G. Magnesium prophylaxis of menstrual migraine: effects on intracellular magnesium. Headache. 1991;31(5):298–301.

4. Mauskop A, Altura BT, Cracco RQ, Altura BM. Intravenous magnesium sulfate relieves migraine attacks in patients with low serum ionized magnesium levels: a pilot study. Clin Sci (Lond). 1995;89(6):633–636.

5. Maizels M, Blumenfeld A, Burchette R. A combination of riboflavin, magnesium, and feverfew for migraine prophylaxis: a randomized trial. Headache 2004; 44: 885– 890.

6. Health Canada. Magnesium [Monograph]. Ottawa (ON): The Department; 2007. Available: http://webprod.hc-sc.gc.ca/nhpid-bdipsn/monoReq.do?id=135&lang=eng (Accessed 1 march 2013).

7. Tarighat Esfanjani A, Mahdavi R, Ebrahimi Mameghani M, Talebi M, Nikniaz Z, Safaiyan A. The effects of magnesium, L-carnitine, and concurrent magnesium-L-carnitine supplementation in migraine prophylaxis. Biol Trace Elem Res 2012; 150(1-3):42-8.

8. Bigal ME, Bordini CA, Tepper SJ, Speciali JG. Intravenous magnesium sulphate in the acute treatment of migraine without aura and migraine with aura. A randomized, double-blind, placebo-controlled study. Cephalalgia 2002; 22(5):345-53.

9. Wang F, Van Den Eeden SK, Ackerson LM, Salk SE, Reince RH, Elin RJ. Oral magnesium oxide prophylaxis of frequent migrainous headache in children: a randomized, double-blind, placebo-controlled trial. Headache 2003; 43(6):601-10.

10. Köseoglu E, Talaslioglu A, Gönül AS, Kula M. The effects of magnesium prophylaxis in migraine without aura. Magnes Res. 2008 Jun;21(2):101-8.

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12. Schiapparelli P, Allais G, Castagnoli Gabellari I, Rolando S, Terzi MG, Benedetto C. Non-pharmacological approach to migraine prophylaxis: part II. Neurol Sci 2010; 31 Suppl 1:S137-9.

13. Pringsheim T, Davenport WJ, Mackie G, et al. Systematic Review: Medications for Migraine Prophylaxis - Section II. Can J Neurol Sci. 2012;39(Suppl. 2):S8-S28.

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Constantine Kaniklidis

Director of Medical Research,

No Surrender Breast Cancer Foundation (NSBCF)

European Association for Cancer Research (EACR)

Hello Ashwini. Basically, multivariate statistic is any kind of analysis that use more than 2 predictors and more than 2 criteria, in one analysis. It means that you have many different elements that help you to predict others. Examples of those are multivariate analysis of variance (MANOVA), and structural equation modeling (SEM). The logistic regression is considered like one of them, but, you have to use one dichotomous or polytomous variable as criteria. The basic assumptions for multivariate analysis are linearity, homocedasticity, and correlation but not multicolinearity between the varaibles... and others that are dependent of the kind of analysis.

There is no evidence base that paleo diet specifically reduces cardio metabolic risk as there has not been enough clinical trials done to evaluate this nor is there any clear data on what the paleo diet was. What there is emerging evidence of, is that processed foods may be increase our cardiometabolic risks. The idea of using evolution as scientific evidence is not sound;evolution does not need to take into account health after children are reared, and most cardio vascular disese occurs after this.

I think the socioeconomic variables included should be based on the theorized mechanism of how you think the social is leading to differences in micro nutrients and/or anthropometry. For example, do you think it is a direct tie of family income to the ability to buy foods with high micronutrient content? Or that educational achievement has improved a person's eating habits through increased knowledge. Or they live in higher social class neighborhood, so have access to better quality food. It could be all of the above and more. Good luck!

There was a review on pulses and diabetes risk in the journaladvances in clinical nutrition (in one of the first few issues.). You may probably find it interesting

HEATH PROMOTION INITIATIVES: THE GOOD, BAD AND THE UGLY

A Mini-Review

BENEFITS

Hundreds of methodologically sound studies have shown that well-designed workplace health promotion programs can be effective in improving health in the domains of smoking cessation, improvement of some eating habits, increased physical activity, reduced excess alcohol use, and improved management of blood pressure and lipids [1,2,5,6]. Furthermore, dozen studies have shown that programs can actually be cost-effective, saving money and sometimes in excess of the costs incurred [3,4].

LIMITATIONS: SMALL SUCCESSSES

(1) But despite the success of these programs, we cannot expect that just any health promotion intervention will either improve health or be cost-effective, since the quality of the delivery of the intervention is critical to success.

(2) And programs based solely on education are unlikely to have much impact: although it's commonplace to believe that if we just informed people about the risks of smoking, excess alcohol, obesity and poor diet on the one hand, and the benefits of exercise, weight control, a nutritious diet, stress management, etc., and then help them learn about their own personal health status, that would be all that was need since people would use their native intelligence reason to readapt to a healthier lifestyle. Unfortunately, as the evidence below suggests, such programs based on these assumptions have been failing for decades. In fact the CDC review [2] referenced below concluded there is “insufficient evidence of effectiveness to recommend” the approach of a health screening plus feedback with no skill building.

(3) It is also important to acknowledge that we have not been successful in developing programs that are predictably successful in helping people in three critical domains:

a. weight loss,

b. increase fitness level, or

c. increase in fruit and vegetable consumption.

These conclusions were also reported in the CDC review [note however that the recent Australian systematic review [7] and a just published RAND Report [8] have contradictory findings on fruit and vegetable consumption, showing efficacy as opposed to the CDC systematic review [2]].

(4) In addition, we must not expect very large efficacy effects from such health promotion initiatives: as the recent Dutch meta-analysis from Anne Rongen and colleagues [9] which reviewed RCTs of 21 interventions in workplace health promotion programs (WHPPs) found, the overall effect of a WHPP was small when considering robust RCTs, with larger effects suggested only in studies of poor/compromised methodology.

The CHALLENGES, AND THE WAY FORWARD

(1) We need to develop, refine and improve initiatives that are culturally, racially, ethnically and faith-sensitive [10]. As I show in my paper on these countervailing factors [11], culture, ethnic and religious beliefs can play a large adverse role to discouraging people from seeking effective interventions: (i) stigmas on body revealment by women in Arab/Muslim populations have engendered a consistently low involvement in breast cancer screening, clinical breast examinations by male professionals, and breast self-examination; (ii) while fatalistic culturally/religious beliefs (that once cancer develops, mortality is certain) disincentivize seeking treatment; and (3) low knowledge and education about the real facts of cancer and other chronic diseases often encourage some people to ineffective alternative modalities.

(2) We need more, and more effective, globally/cross-nationally coordinated and collaborative initiatives that pool and integrate knowledge and successes [12,13,14,15] so that the failures and limitations of already completed interventions are not simply and wastefully repeated in other countries.

(3) We need to recognize, and then develop strategies to overcome what is known as MESSAGE DISSONANCE in health promotion reporting: this phenomenon occurs when despite best efforts at education, subjects are exposed to disorientating mixed and inconsistent messages in the medical and popular media, as when for example, the New York Times Heath Section reports the benefits of coffee or omega-3 fatty acids or moderate drinking, followed in rapid succession but stories that say the opposite, followed again but other divergent results, leaving the consumer thoroughly confused. This happens also with medical reporting sources where the most recent results are reported without consideration or discussion of other existing conflicting results, and with no attempt at what the weight of the evidence shows, as opposed to what any individual study claims (an irrlevancy in evidence-base review and critical appraisal). People can be more influenced by what the assume, usually incorrectly, to be authoritative sources (print and online media) even above and against the messages of national health bodies or their own health professional. And regrettably health professionals themselves show the same patterns of confusions and dissonant reporting, gullibly accepting, say, the negative findings of the USPSTK on prostate cancer PSA testing or the benefits of pre-50 years-of-age mammography, where as I have shown through my own reviews, the USPSTK conclusions (and those, for example of the IOM (Institute of Medicine) on Vitamin D) are in fact in error and founded on severe methodological flaws in their analyses.

(4) Finally, we need some strategies to assure quality control, accountability and consistency of the health promotion information being disseminated where too often school and workplace educators, and nursing, physician, public health, and other stakeholder professionals, may be providing different messages, with no system of review in place for quality assurance and consistency of imparted information; this is the problem of MESSAGE INCONSISTENCY across professionals, rather than MESSAGE DISSONANCE across popular reporting media (print, radio.TV, and online).

METHODOLOGY OF THIS REVIEW

A search of the PUBMED, Cochrane Library / Cochrane Register of Controlled Trials, MEDLINE, EMBASE, AMED (Allied and Complimentary Medicine Database), CINAHL (Cumulative Index to Nursing and Allied Health Literature), PsycINFO, ISI Web of Science (WoS), BIOSIS, LILACS (Latin American and Caribbean Health Sciences Literature), ASSIA (Applied Social Sciences Index and Abstracts), SCEH (NHS Evidence Specialist Collection for Ethnicity and Health) and SCIRUS databases was conducted without language or date restrictions, and updated again current as of date of publication, with systematic reviews and meta-analyses extracted separately. Search was expanded in parallel to include just-in-time (JIT) medical feed sources as returned from Terkko (provided by the National Library of Health Sciences - Terkko at the University of Helsinki). A further "broad-spectrum" science search using Scirus (410+ million entry database) was then deployed for resources not otherwise included. Unpublished studies were located via contextual search, and relevant dissertations were located via NTLTD (Networked Digital Library of Theses and Dissertations) and OpenThesis. Sources in languages foreign to this reviewer were translated by language translation software.

References

1. Wilson MG, Holman PB, Hammock A. A comprehensive review of the effects of worksite health promotion on health related outcomes. Am J Health Promot. 1996;10(6):429–435.

2. Soler R, et al. A systematic review of selected interventions for worksite health promotion: the assessment of health risks with feedback. Am J Prev Med. 2010;38(2 suppl):S237–S262.

3. Aldana S. Financial impact of health promotion programs: comprehensive review of the literature. Am J Health Promot. 2001;1515:296–320.

4. Baicker K, Cutler D, Song Z. Workplace wellness programs can generate savings. Health Aff. 2010;29(2).

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8. Mattke S, Liu H, Caloyeras JP. Workplace Wellness Programs Study. Final Report. Rand Corporation. 2013.

9. Rongen A, Robroek SJ, van Lenthe FJ, Burdorf A. Workplace health promotion: a meta-analysis of effectiveness. Am J Prev Med 2013; 44(4):406-15.

10. Liu J, Davidson E, Bhopal R, et al. Adapting health promotion interventions to meet the needs of ethnic minority groups: mixed-methods evidence synthesis. Systematic review of adapted health promotion interventions. Health Technol Assess 2012; 16(44):1-469.

11. Kaniklidis, C. Cancer, Culture, and Cooperation in the Middle East. [publication pending, 2013. [Available on ResearchGate].

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13. Rice ME. Effective Global Health Promotion Achievements, Tools, and Strategies Used in the Americas Over the Past Decade. Health Promot Pract May 2012 vol. 13 no. 3 313-319.

14. Plumb E, Roe K, Plumb J, Sepe P, Soin K, Ramirez A, et al. The use of international service learning initiatives for global health education: case studies from Rwanda and Mexico. Health Promot Pract 2013; 14(3):334-42.

15. Dixey R. After Nairobi: can the international community help to develop health promotion in Africa? Health Promot Int 2013 Aug 14.