READ This First
If Nothing Else – READ THIS
Many people will read about the HV way of eating and think I am completely mad or over the top, that’s ok, you need to do what is right for you and I need to do what is right for me.
- Stay as You Are
- HV Foods
- Raw Vegan Foods or
- Low Carbohydrate & Low Fat Foods – The Choice is YOURS, just pick it and stick with it!
What you need to remember is my focus is on those who have some form of Metabolic Disorder or Hyperinsulinemia, so for US, we can’t just diet, there is no point in us simply cutting down calories; we can live in negative calories (I have tried this) in other words, we can eat less calories than we have burnt off and still gain weight if those calories are carbohydrate based. It isn’t because we are starving ourselves, if we ate the same calories in low to no carbohydrate foods and foods that were low in fat, we would lose weight in that instance.
The HV way of eating doesn’t even focus on exercise, after years of exercising which is good, and which I would love to do, I was shown that you can still lose the weight and eat healthily without flogging yourself – I know because I have walked the path.
The underlying message with this entire website is simply this:
If you are overweight or obese, and especially if you have Metabolic problems / some form of Hyperinsulinemia:
EAT A LOW CARBOHYDRATE AND LOW FAT DIET
But not without consulting with your Health Care Professional
I am not a main stream Doctor, I am not a Dietician or Nutritionist I am simply one who believes she has been given the key to her own weight loss and realizes that this same key will fit many other doors.
I continually stress that you MUST discuss any dietary changes with your Medical Professional, I, or anyone connected to me, or my websites are not liable for any loss or damage of any kind whether that be physical, psychological, emotional, spiritual or even electronically.
I am not God, nor am I your Health Care Professional; this and all my websites, along will all the information shared on them is offered on an as is basis and is not to be taken as factual or as the only way or the best way.
We all need to find out what is right for us personally, don’t ever just simply believe what another says simply because you deem them more intelligent or more knowledgeable than yourself – they may be wrong sometimes, research things for yourself and NEVER be afraid to ask for a second opinion – Kenzo
Beyond Doubt is about my personal journey back to a slimmer me. Beyond Doubt is NOT here to tell you how you must walk your path, it is here to encourage you to find your own path to health. We are all different and we all need to find what works for us. This isn’t a how too, but rather a reminder that when we find the Ninja within, we will have all our strength and determination at our disposal – The Ninja
All my life I have struggled with weight issues, even looking back at photos of me as a toddler, I was always chubby. In primary school I was obese, in secondary school, I wasn’t too bad, but because I was larger than many, I was still shamed for my size; I was size 14 – 16.
I walked 3 miles to school and 3 miles home most days, saving my bus fare so that I would have spending money at the weekends. I stopped eating breakfast as I realized that the cereal and / or toast (processed carbohydrates) was giving me an insatiable appetite (carbohydrate addiction – inability to manage processed carbohydrates – for more information see the Hyperinsulinemia link in the navigation bar) and I took only one sandwich (more processed carbohydrates) for school lunch hoping to loose weight; this also meant I could save my lunch money for the weekend too.
I ate the same dinner as my siblings and not necessarily in larger quantities yet they were sticks and I wasn’t! Very unfair!
My weight stayed around the same throughout school and after leaving school, I had full-time active jobs.
My twenties and thirties saw me trying very hard to shed the extra pounds, I was either Body Building and practicing Yoga, or Swimming up-to 100 laps once or twice a week along with my Yoga, or using my stationary Bike – I used to cycle 20 miles a day 6 days a week as well as lots of walking.
With such excessive exercise and a very strict diet I was able to keep to 9 st / 126 lbs / 57.15 kg (Normal BMI). I had tried different diets, I even tried fasting 3 days a week and eating salads with some multi-grain bread or pasta (more processed carbohydrates) the other 4 days all of which was excessive. I eventually rested on the Pritikin Diet which is basically no added fats, sugar or oils which was pretty good or so I thought as it still permitted a high carb diet with lean meat and brown rice, all of which I felt I needed because of the amount of exercise I was doing (so more processed carbohydrates)
But in time…………..weight slipped back on.
By my late thirties I was up to 10 st / 140 lbs / 63.50 kg (Normal BMI). I remained that for a couple of years, but then, I left my job and was travelling which was an amazing time of my life but it also meant that it was really hard to stick to a strict diet and exercise plan.
Within 18 months my weight had gone up 2 stone / 28 lbs / 12.70 kg – I was then obese. My rigid eating pattern and rigid exercise regime had slipped, and it was showing, I was eating healthily, but it still wasn’t the right combination for me. Fortunately for me, I had put on the weight evenly so I still looked good, but that wasn’t necessarily a blessing, as still looking good doesn’t encourage you to take action!
I settled in the UK which was very unsettling!!!! and saw another increase in weight, I was fluctuating between 12 stone and 13 stone max. This was not because of a really poor diet as I have always eaten healthily, there may have been some snacks but I certainly wasn’t a couch potato or an excessive junk eater; however, the change in diet and lifestyle took its toll on my weight.
I was still healthy, I have always been healthy which I put down to healthy foods and over 30 years of Yoga and other exercise.
The next 10 yrs saw me averaging out around 12 – 12.7 st with the occasional rise in weight to 13 st.
In 2009 my Scoliosis started to deteriorate, and by the beginning of 2012, I was no longer able to Cycle, Hike, use my AirWalker or even manage my usual Yoga routine which I had done for over 30 years! It was such a loss. My hiking and cycling was my way of being in nature, I didn’t always cycle for miles and my longest cycle in a day was a 55 mile round trip, it was awesome.
Then, May 2012 whilst on my spiritual journey I was shown the High Vibrational Eating (HVE) way. I was prompted to go HV for one whole month and I can honestly say that I dropped two dress sizes in that same month. A 30 yr knee problem vanished and I felt amazing, I was back down to 11 st; so still overweight, but getting there and pretty amazing for 1 month.
Although the HVE way is full of tasty foods which I love, it was hard sticking to it 100% of the time when everyone else was cooking and wanting you to join them and eat what they were eating. Smelling cooked foods often used to bring back so many good memories of happy times as well as enjoyable tastes. Then of course, every time we went out for the day, it was difficult when everyone else wanted a Chinese or Fish & Chips and I wanted to get a salad! So although I remained strict with my HVE for a long time, as time went on, I became a little blasé and found myself veering from 100% HV on some days, not all days but some days and this may have been by simply adding a fresh bread roll and this, (being processed carbohydrates) was enough to put the weight back on, unbelievable, it is hard to believe that something so simple could and did put on all the weight again; and most of the time the veering from 100% was just to compromise and make it easier for others.
Some days I would have 100% HV, other days it may be 90/10 with 90% being HV. At that time, I didn’t understand how eating the odd multi-grain bread roll, or eating the odd rice or pasta dish (all being processed carbohydrates) could put on so much weight as it had nothing to do with calorie intake. I found people who knew I was now eating Raw and Vegetarian / Vegan saying things like: You can’t be a Vegan or You can’t be mainly Raw, and I knew that is was because they deemed me too fat to be on such diets!
Since 2012, I have known that I need to remain faithful to the HVE way as much as I possibly can; 2013 – early 2016, I saw my weight go up and down from 11 st – 12 stone and occasionally just over, so still an improvement.
April 2016 I was back on the 100% HVE every day so weight was dropping off, I was due to have a double Prophylactic Mastectomy in May, overseas, so I needed to have my bloods checked and have an ECG. My in-depth blood results reflected that EVERY single reading was within the normal range which was great for my pending surgery. (I will add the results to the website at some time, they are in Spanish but you can see the results are normal and many of the words are similar to English). The Oncologist Surgeon and Heart Specialist were amazed by both my blood results and my ECG. The Heart Specialist said that going by my blood results and my ECG, I was biologically at-least 20 yrs younger than my age which was really nice to hear at 54 years old. So despite the occasional lapse, my HVE was working for me without having to flog myself with exercise.
In late 2016 due to the fact that I had managed to remain very strict with my HVE, I was pleased to see my weight had dropped down to 10.7 st, I was so pleased, just 7 lbs away from my normal BMI! At this time I was still overseas and due to come back to the UK which was such a disruptive time. I had had the double Mastectomy and also taken the time to visit a Spine Specialist / Surgeon in regards to my Scoliosis and had started to accept that due to the deterioration in my Scoliosis, I would be needing a wheelchair. Many people I am sure would wonder if the HV way was contributing to the deterioration in my spine, but it wasn’t; it had been deteriorating for a few years prior to my HVE and I was aware that if I didn’t stay on my HVF’s I did in fact have more pain.
Arriving back in the UK in winter wasn’t the best but it was nice to be back for Christmas and it was nice to have a wheelchair waiting for me. I held onto the idea of eventually being an active wheelchair user, but to-date, that just isn’t happening, my neck will not permit be to put any strain on it, so my active wheelchair use is reduced to getting around the supermarket; because the floors are smooth it places less resistance on the chair and on my neck, THAT is about as much exercise as I can currently manage – not what I am used to!
So needless to say, with no real exercise and adding the odd bread roll (processed carbohydrates), the odd sweet potatoes (more carbohydrates) etc to my HVE, the weight went back on; and 9 months later, I found myself right back up at 13 st – courtesy of my own stupidity for eating PROCESSED CARBOHYDRATES!
Many will be convinced that I spent 9 months binge eating, but that is not the case at all, one thing I have had to learn over the years is that all it takes for me personally, is one or two things a day that are not HV foods (especially if they are processed carbohydrates) and that is enough to see my weight increase rapidly, it has nothing to do with calories or fat intake.
My learning has been that my body does not function at its best if I eat carbohydrates, but especially processed carbohydrates because of one form or another of Hyperinsulinemia; so if I eat carbohydrates, my body then craves carbohydrates so I personally need to be very limiting with carbohydrates in general; this is a learning curve that I have had to embrace and if I hadn’t gone through this myself, I would not be able to be here today helping others, helping you, go through the same.
Part of my learning over the last few years has been about Hyperinsulinemia. It is this learning that opened my eyes and gave me the understanding as to why I have had a hard time over the years keeping off the weight. But this has also been my blessing, as this information has permitted me to understand how and why SOME people are continually obese, why SOME people don’t seem to lose weight no matter what and why SOME people who eat healthily can still be fat.
So if you are struggling with your weight, or are one of these people who has always been over-weight know matter what; there is a reason, and for many, I believe it will be Hyperinsulinemia in one form or another. For me, I know that carbohydrates are my worst enemy, even one bread roll a day is enough to set my body off into a negative cycle which will add weight to the scales and guarantee me ending up right back at 13st, but for all you out there, it may be different and you must find out for yourselves what your problem is.
(If you want to read more about Hyperinsulinemia follow the link in the navigation bar).
But now………………………as I write this, it is time to take the knowledge and personal experience that I now have and take back control and get myself back to a normal BMI, whilst using that same knowledge to keep me there; and that is what this website is about.
I wanted to publicise my journey back to the real me because I know it will help some and encourage others, I know it will be the boost that some need and for that reason alone, it has been worth carrying every pound of weight because without it, I wouldn’t be here today helping you.
The difference between me and many of you is simply this, I have walked the path and discovered what my body requires and what it does not require, I have been up and I have been down, both on the scales and emotionally as I have had to continually wrestle with weight gain. But now, now it is just a case of deciding to go Beyond Doubt – Allowing NO Uncertainty.
So if you have a weight problem and have discussed this with your Doctor or Dietician and have been given the go-ahead, join me on my journey, stay strong, find the Ninja within and follow that dream, you are not alone, you are never alone.
We can all be our biggest enemy, even you, and in that case, it is you that your Ninja needs to fight, you must be willing to climb Beyond Doubt – Allowing NO Uncertainty.
Raw or High Vibrational Eating - Is there a Difference?
Raw or High Vibrational Eating?
Is there a Difference?
The answer is clearly YES. Whilst a Raw Vegan diet is mostly High Vibrational there are some foods which the Raw Vegan Diet permits you to eat that I have been shown are not H.V. An example of this could be commercial peanut butter, because of the processing and additives it is said to be less than High Vibrational. Pure juices are another example, if sold in glass that would be considered more Vibrational than one sold in a carton but not as High in Vibration as freshly squeezed juice. Dried fruit is often used in the Raw Vegan Diet, but due to the additives or even the oil it is not considered High Vibrational.
This could be seen as purely splitting hairs and in one way it is, but what we all need to do is look at why we are on either Raw or H.V.E. we need to look at what is not only right for us personally, but what is also achievable.
Will it lessen the ascension of your spiritual body if you stick with Raw as opposed to HVF? It probably will, HOWEVER, whether it would lessen it to a noticeable degree is debatable and not worth arguing about. What we need to focus on is that even the Raw Vegan Diet is going to make a massive change to your body, mind AND SPIRIT. It is certainly NOT less than the H.V.F’s simply because there is such an overlap.
For me personally, I know that I am required to eat the H.V. way as much as possible, but there are times when it is not possible, for example; naturally dried fruit, that is fruit dried in the sun with NO additives and no oil added to them is very limited, it can be expensive and not always easy to come by and for this reason, I do what I can but try to stay ATLEAST on the Raw Vegan Diet. There are times I get it wrong, there are times I choose to eat something that I call dead based on its low vibration, especially if I am at someone else’s home, but ultimately I know that I need to continually work towards perfecting my diet to be purely High Vibrational.
Always consult your Doctor or Dietician before making ANY dietary changes.
Hyperinsulinemic Obesity (HO)
The Obese, The Over-Weight & Hyperinsulinemia
Obesity and overweight is a growing concern, not only in the U.S. but worldwide. With today’s fast foods and junk foods being so prevalent, and often so cheap, it stands to reason that not only today’s generation of young people, but ALL people are at greater risk of Coronary Heart Disease (CHD) or any other Cardio Vascular Disease (CVD) to say the least.
Many individuals make improper food choices based on their senses such as taste or smell, some lack education on healthy eating habits, while others base their choices on either available foods or affordable foods.
In all cultures we will find the obese, the overweight, not one culture is without this group within their population. If there were any cultures that did not have overweight or obese individuals we would be able to compare that cultures diet to the rest of the world.
Obesity and being overweight is a precursor to ill health, not only in later life but right through life, with the added likelihood of ill health worsening in later life. That doesn’t mean that people who are not overweight are not at risk, some are for other reasons, but what it does mean is that overweight and obese individuals are MORE at risk of suffering ill health.
It is usually assumed that obese or over-weight people eat the wrong foods, eat too much food, are lazy, don’t exercise, have no self-control and do not care about their appearance. Some obese people may fit that description, but not all, some could successfully take control of their weight issues with the help of education and support. YET, this doesn’t describe ALL obese individuals.
Some obese individuals are out of control, they do lack self-discipline and they are eating the wrong foods. HOWEVER, I would also like to add that some are out of control because of a biological in-balance, their lack of self-discipline is due to that same biological in-balance and they are eating the wrong food because they do not realize to what extent the food is wrong for them. Here, I am not simply talking about unhealthy cakes, deserts and biscuits per sae, I am talking about a specific food group being wrong for them. Many of these people crave the very foods that keep them obese or over-weight NOT because they are weak but because of a condition, a biological condition that prevents their bodies from functioning as it does in the normal individual.
Many individuals go through life not realizing that they can overcome obesity and they can overcome it simply and easily by reducing significantly, or eliminating one food group.
This website doesn’t promise to be the answer to obesity per sae, but it will help many obese and overweight individuals.
There are a group of obese or overweight individuals who have tried diets, who have tried increasing exercise, who have done this and that without successful weight loss. They may have lost some weight, they may have lost a lot of weight, but overtime, the weight simply goes straight back on. They may have had counselling for comfort eating, they may have had counselling to encourage behavioural changes, but still, this same group of individuals continue to struggle to maintain sufficient weight loss to assist in better health. This group of individuals may be suffering from a condition known as Hyperinsulinemic Obesity in one form or another, this page looks at why that is, it addresses some of the issues around obesity and over-weight in this specific group.
When you look around at the available literature, there appears to be a gap in the literature on Hyperinsulinemia. There appears to be little information around to help these individuals, it would seem that they have simply been categorized by many as out of control and left to it.
I am one such individual. Having grown up constantly struggling to maintain a healthy weight I know only too well what it feels like being seen as obese or overweight.
Looking back at family photos, you can clearly see that my siblings where both slim and I was obese. We ate the same foods, we had the same helpings, we all exercised, so why was that?
I remember at the age of 10 years the Doctor telling my mum that I was too fat and needed to go on a diet. I was permitted to eat my normal breakfast and lunch and while the rest of the family sat down to a cooked dinner, I was given a plate with some Rivita crackers on it and even those were limited. I can still remember the psychological affect that had on me. I was indirectly made to feel un-acceptable, not good enough and bad to say the least. I felt rejected not only by some of my family, but by society. I had become a joke, a laughing stock to others. I was teased because of my weight, called un-kind names and often made fun of; my struggle to maintain weight or lose weight went right through into adult-hood.
Over the years, after trying many diets, eating healthily and excessive exercising I always returned to approximately what I had been. It didn’t seem to matter how many or how few calories I ate, it didn’t matter that I cycled 20 miles five or six times a week and only ate as many calories as I had burned off, the weight would always find its way back on.
It wasn’t until 2012 that I discovered a way of eating that was to change my life. I was 50 years old, 5ft 3in, a size 18 at the top and 16 at the bottom which doesn’t sound too bad, I carried my weight very evenly, however, I was weighing 13 stone, (182lbs / 82.55 kg) which gave me a BMI of 32.2; I was registering as obese. It is that same way of eating that I have shared on this website, it is called High Vibrational Eating.
Hyperinsulinemia & Hyperinsulinemic Obesity
The following information has been taken directly from other sources and a link has been provided for your convenience to the original source.
Hyperinsulinemia, or hyperinsulinaemia is a condition in which there are excess levels of insulin circulating in the blood than expected relative to the level of glucose. While it is often mistaken for diabetes or hyperglycaemia, hyperinsulinemia can result from a variety of metabolic diseases and conditions. While hyperinsulinemia is often seen in people with early stage type 2 diabetes mellitus, it is not the cause of the condition and is only one symptom of the disease. Type 2 diabetes only occurs when pancreatic beta-cell function is impaired. Hyperinsulinemia can be seen in a variety of conditions including diabetes mellitus type 2, in neonates and in drug induced hyperinsulinemia. It can also occur in congenital hyperinsulism, including nesidioblastosis.
Hyperinsulinemia is associated with hypertension, obesity, dyslipidemia, and glucose intolerance. These conditions are collectively known as Metabolic syndrome. This close association between hyperinsulinemia and conditions of metabolic syndrome suggest related or common mechanisms of pathogenicity. Hyperinsulinemia has been shown to “play a role in obese hypertension by increasing renal sodium retention”.
In type 2 diabetes, the cells of the body become resistant to the effects of insulin as the receptors which bind to the hormone become less sensitive to insulin concentrations resulting in hyperinsulinemia and disturbances in insulin release. With a reduced response to insulin, the beta cells of the pancreas secrete increasing amounts of insulin in response to the continued high blood glucose levels resulting in hyperinsulinemia. In insulin resistant tissues, a threshold concentration of insulin is reached causing the cells to uptake glucose and therefore decreases blood glucose levels. Studies have shown that the high levels of insulin resulting from insulin resistance might enhance insulin resistance.
Studies on mice with genetically reduced circulating insulin suggest that hyperinsulinemia plays a causal role in high fat diet-induced obesity. In this study, mice with reduced insulin levels expended more energy and had fat cells that were reprogrammed to burn some energy as heat.
Hyperinsulinemia in neonates can be the result of a variety of environmental and genetic factors. If the mother of the infant is a diabetic, and does not properly control her blood glucose levels, the hyperglycemic maternal blood can create a hyperglycemic environment in the fetus. To compensate for the increased blood glucose levels, fetal pancreatic beta cells can undergo hyperplasia. The rapid division of beta cells results in increased levels of insulin being secreted to compensate for the high blood glucose levels. Following birth, the hyperglycemic maternal blood is no longer accessible to the neonate resulting in a rapid drop in the newborn’s blood glucose levels. As insulin levels are still elevated this results in hyperinsulinemia. To treat the condition, high concentration doses of glucose are given to the neonate as required maintaining normal blood glucose levels. The hyperinsulinemia condition subsides after one to two days. (http://en.wikipedia.org/wiki/Hyperinsulinemia)
It is proposed that chronic hyperinsulinemia is largely responsible for hunger, cravings and weight gain observed in many obese. This form of obesity can be treated by decreasing frequency of daily intake of carbohydrates to one well-balance meal each day and allowing for additional meals that are low in fat, low carbohydrates and high fiber. Animal experimentation and epidemiological evidence support the role of chronic hyperinsulinemia as a major factor in obesity and accounts for the frequent failures of diet and behavioral modification programs. Chronic hyperinsulinemia upsets metabolic balances and favors anabolic metabolism; fosters carbohydrate cravings; promotes insulin resistance which further promotes anabolic metabolism; and insulin resistance in turn exacerbates chronic hyperinsulinemia. This vicious cycle maintains excess weight and defeats diet and behavioral modification attempts to treat obesity. An eating program focused on reduction of chronic hyperinsulinemia coupled with appropriate exercise and behavior modification can successfully and permanently bring down cravings, hunger and body weight (http://www.ncbi.nlm.nih.gov/pubmed/7935072)
Anabolic processes tend toward “building up” organs and tissues. These processes produce growth and differentiation of cells and increase in body size, a process that involves synthesis of complex molecules. Examples of anabolic processes include the growth and mineralization of bone and increases in muscle mass. Endocrinologists have traditionally classified hormones as anabolic or catabolic, depending on which part of metabolism they stimulate. The classic anabolic hormones are the anabolic steroids, which stimulate protein synthesis and muscle growth, and insulin. The balance between anabolism and catabolism is also regulated by circadian rhythms, with processes such as glucose metabolism fluctuating to match an animal’s normal periods of activity throughout the day. (http://en.wikipedia.org/wiki/Anabolism)
Anabolic steroids, technically known as anabolic-androgenic steroids (AAS), are drugs that are structurally related to the cyclic steroid ring system and have similar effects to testosterone in the body. They increase protein within cells, especially in skeletal muscles. Anabolic steroids also have androgenic and virilizing properties, including the development and maintenance of masculine characteristics such as the growth of the vocal cords, testicles (primary sexual characteristics) and body hair (secondary sexual characteristics). The word anabolic comes from the Greek ἀναβολή anabole, “that which is thrown up, mound”, and the word androgenic from the Greek ἀνδρός andros, “of a man” + -γενής -genes, “born”.
Anabolic steroids were first made in the 1930s, and are now used therapeutically in medicine to stimulate bone growth and appetite, induce male puberty and treat chronic wasting conditions, such as cancer and AIDS. The American College of Sports Medicine acknowledges that AAS, in the presence of adequate diet, can contribute to increases in body weight, often as lean mass increases and that the gains in muscular strength achieved through high-intensity exercise and proper diet can be additionally increased by the use of AAS in some individuals.
Health risks can be produced by long-term use or excessive doses of anabolic steroids. These effects include harmful changes in cholesterol levels (increased low-density lipoprotein and decreased high-density lipoprotein), acne, high blood pressure, liver damage (mainly with oral steroids), and dangerous changes in the structure of the left ventricle of the heart. Conditions pertaining to hormonal imbalances such as gynecomastia and testicular atrophy may also be caused by anabolic steroids (http://en.wikipedia.org/wiki/Anabolic_steroid)
Insulin is a peptide hormone, produced by beta cells in the pancreas, and is central to regulating carbohydrate and fat metabolism in the body. It causes cells in the skeletal muscles, and fat tissue to absorb glucose from the blood.
Insulin stops the use of fat as an energy source by inhibiting the release of glucagon. Except in the presence of the metabolic disorder diabetes mellitus and metabolic syndrome, insulin is provided within the body in a constant proportion to remove excess glucose from the blood, which otherwise would be toxic. When blood glucose levels fall below a certain level, the body begins to use stored sugar as an energy source through glycogenolysis, which breaks down the glycogen stored in the liver and muscles into glucose, which can then be utilized as an energy source. As a central metabolic control mechanism, its status is also used as a control signal to other body systems (such as amino acid uptake by body cells). In addition, it has several other anabolic effects throughout the body (http://en.wikipedia.org/wiki/Insulin)
The theoretical minimal level of carbohydrate (CHO) intake is zero, but CHO is a universal fuel for all cells, the cheapest source of dietary energy, and also the source of plant fiber. In addition, the complete absence of dietary CHO entails the breakdown of fat to supply energy [glycerol as a gluconeogenic substrate, and ketone bodies as an alternative fuel for the central nervous system (CNS)], resulting in symptomatic ketosis. Data in childhood are unavailable, but ketosis in adults can be prevented by a daily CHO intake of about 50 g. This value appears to approximate the quantity of glucose required to satisfy minimal glucose needs of the CNS and during starvation. The Group therefore concluded that the theoretical minimum intake of zero should not be recommended as a practical minimum.…about 100 g of glucose/d are irreversibly oxidized by the brain from the age of 3–4 y onward. However, this excludes recycled carbon, gluconeogenic carbon, for example from glycerol, and it does not account for glucose used by other non-CNS tissues. For example, in the adult, muscle and other non-CNS account for an additional 20–30 g of glucose daily. For this reason a safety margin of 50 g/d is arbitrarily added to the value of 100 g/d and the practical minimal CHO intake set at 150 g/d beyond the ages of 3–4 y.”
Thus, although carbohydrate could theoretically be eliminated from the diet, the recommended intake of 150 g/d ensures an adequate supply of glucose for the CNS. However, it appears that during starvation (a condition in which the intakes of carbohydrate, protein, and fat are eliminated), an adequate amount of substrate for the CNS is provided through gluconeogenesis and ketogenesis (6). The elimination of dietary carbohydrate did not diminish the energy supply to the CNS under the conditions of these experiments. Second, carbohydrate is recommended to avert symptomatic ketosis. In the largest published series on carbohydrate-restricted diets, ketosis was not typically symptomatic (7).
The most direct way to determine whether carbohydrate is an essential nutrient is to eliminate it from the diet in controlled laboratory studies. In studies involving rats and chicks, the elimination of dietary carbohydrate caused no obvious problems (8–,12). It was only when carbohydrate restriction was combined with glycerol restriction (by substituting fatty acids for triacylglycerol) that chicks did not develop normally (13). Thus, it appears that some minimum amount of a gluconeogenic precursor is essential—for example, glycerol obtained from fat (triacylglycerol) consumption. More subtle abnormalities from carbohydrate elimination might not have been observed in these studies. In addition, the essentiality of some nutrients is species-specific; therefore, these studies do not provide convincing evidence that elimination of dietary carbohydrate is safe in humans (4).
The usual way to discover the essentiality of nutrients is through the identification of specific deficiency syndromes (4). I found no evidence of a carbohydrate deficiency syndrome in humans. Protein deprivation leads to kwashiorkor, and energy deprivation leads to marasmus; however, there is no specific carbohydrate deficiency syndrome. Few contemporary human cultures eat low-carbohydrate diets, but the traditional Eskimo diet is very low (≈50 g/d) in carbohydrate (2). It is possible that if more humans consumed diets severely restricted in carbohydrate, a carbohydrate deficiency syndrome might become apparent.
When carbohydrates are eliminated from the diet, there is a risk that intakes of vitamins, minerals, and perhaps yet unidentified beneficial nutrients provided by carbohydrate-rich foodstuffs (eg, fiber) will be inadequate. There are case reports of extreme dieters who probably developed deficiencies.
One dieter who only ate cheese, meat, and eggs (no vegetables) was reported to have developed thiamine-deficient optic neuropathy (14). Another dieter may have developed a relapse of acute variegate porphyria (15). However, most of the current low-carbohydrate, weight-reducing diets advocate the consumption of low-carbohydrate vegetables and vitamin supplements.
Although there is certainly no evidence from which to conclude that extreme restriction of dietary carbohydrate is harmless, I was surprised to find that there is similarly little evidence to conclude that extreme restriction of carbohydrate is harmful. In fact, the consequential breakdown of fat as a result of carbohydrate restriction may be beneficial in the treatment of obesity (7). Perhaps it is time to carefully examine the issue of whether carbohydrate is an essential component of human nutrition.
American Journal of Clinical Nutrition (http://ajcn.nutrition.org/content/75/5/951.2.full)
As many as seventy-five percent of those who are overweight, and many normal-weight individuals as well, are carbohydrate addicted. Though many people may suspect there is a physical imbalance that makes them crave carbohydrates and put weight on easily, the underlying cause of their cravings and weight struggles often goes undiagnosed and untreated.
Carbohydrate addiction is caused by an imbalance – an over release of the hormone, insulin, when carbohydrate-rich foods are eaten. Among its many jobs, insulin signals the body to take in food (it has been called the “hunger hormone”) and, once the food is consumed, signals the body to store the food energy in the form of fat.
Too much insulin results in too strong an impulse to eat, too often, and a body that too readily stores food in the form of fat.
The scientific term for this condition is post-prandial reactive hyperinsulinemia which means too much insulin is released after eating. Over time, people who are hyperinsulinemic become insulin resistant, that is, the cells in their muscles, nervous systems, and organs start to close down to the high levels of insulin in their blood. Insulin is no longer able to open the doors to these cells and allow food energy (blood sugar or glucose) to enter. At this point, one may experience symptoms of low-blood sugar levels (hypoglycemia) including irritability, shakiness, tiredness, intense cravings, confusion, and headaches. Since the blood sugar cannot easily enter the muscles, nervous system, or organs, much of the food energy gets channeled into the fat cells and weight gain comes easily. Over time, however, as high insulin levels continue, even the fat cells can shut down and the blood glucose gets trapped in the blood stream bringing on the condition known as adult-onset diabetes.
At this time, there is no accepted blood test to definitively determine whether or not you have a carbohydrate addiction. Fasting insulin levels do not necessarily predict how your body will react after eating carbohydrate-rich foods and glucose tolerance tests use highly sweetened drinks that are not the equivalent of typical carbohydrate-rich meals. If you are carbohydrate addicted, however, chances are you know that something different about the way in which your body responds to starches, snack foods, junk food, and sweets (http://www.carbohydrateaddicts.com/cadfnd.html)
Although carbohydrate addiction is caused by an imbalance – an over release of the hormone, insulin when carbohydrates are taken into the body, the cause itself isn’t the insulin. The cause is the inability to cope or manage the carbohydrates, which in turn results in the over release of insulin.
By restricting the intake of carbohydrates, it stands to reason that our bodies should then be able to lower the amount of insulin released, avoiding carbohydrate cravings to say the least. When we restrict the intake of carbohydrates we force the body to metabolise fat instead of glucose. By consuming only low-fat foods, we further enable the body to metabolize stored fat.
The more carbohydrates we take in, (either simple or complex, the simple carbohydrates are known as sugars, the complex carbohydrates are known as starches, but they are also made up of chains of glucose) the more insulin we produce, in a normal individual, the body would metabolize this accordingly. When the blood-sugar levels dropped down, so would the insulin levels.
Where-as the normal person can eat carbohydrate and it will be absorbed efficiently into the body to produce glucose, in the Hyperinsulinemic individual, the carbohydrates are NOT broken down and used efficiently as glucose, as the body is prevented from absorbing the glucose it is then stored as fat. The results being, apparent, low blood-glucose levels, also known as Hypoglycaemia. This in-itself, forges carbohydrate cravings which once again, fail to be used adequately and so result in being stored as fat.
Hypoglycaemia is usually brought on by a ‘fasting’ state, whether a deliberate fast or by an extended period between meals. Usually this can be anything from 3-5 hours after eating. In the normal individual, Hypoglycaemia can be reversed adequately and quickly by the oral administration of carbohydrates. In the Hyperinsulinemic individual, the apparent, Hypoglycaemic symptomology can present itself much sooner, even shortly after a meal. This would suggest that a Hypoglycaemic test would prove ‘negative’ and should indeed prove ‘positive’ reflecting a normally raised blood-glucose level due to the consumption of food, HOWEVER, the symptomology would be of hypoglycaemia due to the lack of absorption of glucose.
Due to the constant cycle of carbohydrate ‘fake’ deficiency (due to the over production of insulin) which fools the body into believing it needs to force the individual to eat carbohydrate via the use of cravings, a constant increase of weight is apparent or a constant in-ability to lose weight and keep it off occurs.
In the Hyperinsulinemic individual, it does matter how much exercise they do, as long as they are consuming carbohydrates, they will fail to lose weight. Also, because of the amount of endogenous insulin available in the body on a regular basis, there is also the natural ability to be able to put on muscle mass, imitating testosterone abilities.
Hyperinsulinemic individuals are more likely to be those individuals who have what is called a ‘chunky’ appearance without necessarily it being from muscular statute.
Hyperinsulinemic individuals are commonly seen as plump or obese from childhood, with little ability to lose weight. They can be wrongly labelled ‘lazy’ or ‘lacking self-discipline’. The Hyperinsulinemic individual has no control per sae over their weight, they have a biological dysfunction as opposed to a psychological dysfunction.
Where-as for the average normal person, a very restricted carbohydrate diet may not be sufficient to maintain a balance between insulin and glucose, in the Hyperinsulinemic individual, a very restrictive carbohydrate diet may prove useful. Such diet may be constructive in the regulation of insulin which may also lead to weight loss.
It is recognized that the Hyperinsulinemic individual must be made aware of the importance, and necessity of a balance diet to ensure adequate absorption of essential vitamins and minerals etc.
Impaired glucose metabolism was demonstrated to be a predictor of development of congestive heart failure in a large community-based sample of elderly men (Ingelsson et al 2005). Surprisingly, when insulin sensitivity and the impaired glucose tolerance were analyzed as co-variates, obesity was no longer a significant predictor of the subsequent development of congestive heart failure. This suggests that obesity may be a coincidental predictor of congestive heart failure and may simply be a marker of insulin resistance, which is compensated for by hyperinsulinemia.
Ingelsson et al (2005) suggest that the hyperinsulinemia associated with impaired glucose metabolism represents a risk factor through several possible mechanisms. Insulin acts as a growth factor in the myocardium as shown by increased myocardial mass and decreased cardiac output in rats exposed to sustained hyperinsulinemia (Holmang et al 1996).
Hyperinsulinemia leads to sodium retention (DeFronzo et al 1975) which may exacerbate subclinical myocardial dysfunction due to blood volume expansion. Hyperinsulinemia leads to sympathetic nervous system activation (Anderson et al 1991) which is a presumed causal factor for congestive heart failure (Kannel and Belanger 1991; Bell 2003). Insulin resistance is related to increased effectiveness of angiotensin II on blood pressure (Gaboury et al 1994) and cellular hypertrophy and collagen production (Sartori et al 2004) in individuals with hypertension, leading to myocardial hypertrophy and fibrosis (Bell 2003) and likely subsequent congestive heart failure
Hyperinsulinemia can be seen as a postprandial metabolic dysfunction seen in the pre-diabetic insulin resistant state.
Although food cravings are a major part of Hyperinsulinemia, this isn’t the only cause for food cravings, so food cravings alone cannot be isolated as a sign of Hyperinsulinemia. There are many causes of such food cravings ie: poor diet, parasites, excessive yeast, bacteria, Candida, stress, allergies, food additives, chemicals, poor eating habits and deficiency of vitamins etc. so cravings alone are not enough to suggest that someone has Hyperinsulinemia.
Hyperinsulinemia may show itself with any or all of the following:
Coronary Vascular Disease
High Blood Pressure
High Cholesterol – (raising of the LDL and lowering of the HDL
Easy Weight Gain
Inability to Lose Weight
Inability to Keep Weight Off
Inability to Control Eating Habits
Feelings of Hunger Even After Eating
Strong Carbohydrate Cravings – (can be complex or simple carbohydrates including alcohol))
Lack of Energy or Stamina Leading to the Feeling of ‘I Need Food’
Symptomology of Hypoglycaemia – (low blood sugar)
Encouraging the body to metabolize fats instead of glucose is called Ketosis, this process begins when insulin levels are low which is usually when blood glucose levels are low, usually prior to eating. Reduced insulin levels induce a process called Lipolysis, which consumes fat to produce Ketones.
If we briefly look at the Atkins diet, we can see that the diet is based on the same pretences, that is, that we need a low or restricted carbohydrate diet in order to lose weight.
The initial stage of the Atkins Diet is referred to as the induction phase and is considered a ketogenic diet. In ketogenic diets there is production of ketones that contribute to the energy production in the Krebs cycle. Ketogenic diets rely on the insulin response to blood glucose. Insulin is a hormone produced by beta-cells in the pancreas in response to high levels of blood glucose (i.e. after digestion of a carbohydrate meal). The main function of insulin is to shuttle glucose from the blood to peripheral tissues, where they will be needed for fuel or stored as fat. Thus, insulin is a regulator of blood glucose that is too high.
Because ketogenic dieters eat few carbohydrates, there is no glucose that can trigger the insulin response. Therefore, the body must seek an alternate fuel source to fulfill its metabolic needs. During this diet, the main sources of fuel for human cells (glucose) is now at less than adequate supply, cells must take alternate steps to convert stored fuel to glucose. Other than carbohydrate ingestion (which is directly converted into glucose and then immediately available for use as fuel when it enters the blood), the cells must rely on glucose production from conversion of either protein (amino acids) or stored fat.
When blood levels of glucose are low, regulating hormones are released to signal for the need to elevate blood sugar. This is in contrast to the actions of insulin. Since the body is less able to compensate for a state of hypoglycemia, than it is for hyperglycemia, hormones (growth hormone, epinepherine, cortisol, and glucagon) are released causing a cascade resulting in glycogen release from the liver and adipose (fat) cell conversion of triacylglycerol to fatty acids.
Blood glucose levels have to decrease to less than 3.58 mmol/L (64.5 mg/dl) for growth hormone, epinephrine, and glucagon to be released to maintain energy metabolism. In the adipose cells, growth hormone and epinephrine initiate the triacylglycerol to be broken down to fatty acids. These fatty acids go to the liver and muscle where they should be oxidized and give acetyl-CoA that enters the Krebs cycle directly. However, the excess acetyl-CoA in the liver is converted to ketones (ketone bodies), that are transported to other tissues. In these tissues they are converted back into acetyl-CoA in order to enter the Krebs cycle. Glucagon is produced when blood glucose is too low, and it causes the liver to start breaking glycogen into glucose. Since the dieter does not eat any more carbohydrates, there is no glycogen in the liver to be broken down, so the liver converts fats into free fatty acids and ketone bodies, and this process is called ketosis. Because of this, the body is forced to use fats as a primary fuel source.
Although there has been some research done throughout the twentieth century, most directly relevant scientific studies, both those that directly analyze the Atkins Diet and those that analyze similar diets, have occurred in the 1990s and early 2000s and, as such, are relatively new.
Researchers and other experts have published articles and studies that run the gamut from promoting the safety and efficacy of the diet, to questioning its long-term validity, to outright condemning it as dangerous. A significant early criticism of the Atkins Diet was that there were no studies that evaluated the effects of Atkins beyond a few months. However, studies began emerging in the mid-to-late-2000s which evaluate low-carbohydrate diets over much longer periods, controlled studies as long as two years and survey studies as long as two decades.
In addition to research on the efficacy of Atkins and other low-carbohydrate diets, some research has directly addressed other areas of health affected by low-carbohydrate diets. For example, contrary to popular belief that low-carbohydrate diets damage the heart, one study found that women eating low-carbohydrate, high-fat/protein diets had the same or slightly less risk of coronary heart disease, compared to women eating high-carbohydrate, low-fat diets. Other studies have found possible benefits to individuals with type 2 diabetes, cancer, and epilepsy. One study comparing two levels of low-carbohydrate diets (ketogenic—the lowest carbohydrate level—and non-ketogenic) found that both had positive effects in terms of insulin sensitivity, weight loss, and fat loss while the ketogenic diet showed slightly higher risks of inflammation and somewhat lower perceived levels of vigor, described as “potentially harmful metabolic and emotional side-effects” (although it should be noted that one of the researchers of this study, Barry Sears, markets The Zone as a competing low-carbohydrate diet).
A 2007 study done at Stanford University Medical School, The A to Z Weight Loss Study, compared the Atkins Diet with the Zone, Ornish, and LEARN diets in a randomized group of 311 obese premenopausal women over a period of 12 months. The study found that weight loss was significantly higher for the Atkins Diet compared to the other three diets. Secondary factors such as HDL-C, triglyceride levels, and systolic blood pressure were also found to have improved to healthier levels compared to the other diets.
A 2012 study done at Boston Children’s Hospital compared a very low carbohydrate diet (the Atkins Diet) with a low fat, high carbohydrate diet, and a low glycemic index diet. Reduction of the resting metabolic rate as a result of dieting, a key factor in the failures of dieting, was the least in the very low carbohydrate diet. In addition, measured total energy expenditure in the patients was the highest in the very low carbohydrate diet, suggesting that a very low carbohydrate diet would be the most likely to produce a sustained weight loss. A possible negative side effect was that C-Reactive Protein levels, a marker for possible future cardiovascular disease, trended somewhat higher in the very low carbohydrate diet.
In January 2004, the BBC Two science program Horizon broadcast the results of experiments comparing Atkins to other diets. Dr. Joe Millward of the University of Surrey, who headed up the research, concluded that the Atkins dieters lost weight because they were eating fewer calories, just as people on low-fat diets do. The program also attributed Atkins weight loss to the fact that carbohydrates are the least filling food. Professor Arne Astrup, of the Royal Veterinary & Agricultural University in Copenhagen, conducted a study comparing a group of people on a high protein diet to another group on a high carbohydrate diet. According to Astrup, the group eating more protein lost significantly more weight because protein is more easily filling, and thus members of that group consumed fewer calories, even though they had free access to whatever food they wanted. (http://en.wikipedia.org/wiki/Atkins_diet)
There is some controversy as to whether or not the Atkins diet is good. The diet permits the individual to lose weight and then raise the carbohydrates to a level where they can maintain their weight. This would seem appropriate to the normal individual, however, for the individual with Hyperinsulinemia, it would stand to reason that by increasing the level of carbohydrates, it would, once again stimulate the over production of insulin.
With this is mind, it is perhaps worth considering sticking to a minimum of 12 grams per day of carbohydrates which is what was stated to be the average amount of carbohydrates the Eskimos live on, these carbohydrates would need to be gained purely from natural sources eg: fruit, salad, vegetables.
It could be seen useful to use the Atkins diet for advice on recipes and for using their charts for grams of carbohydrates within certain food lists.
However, for the Hyperinsulinemic individual, it would seem more appropriate to remain on the Atkins week one, the Initial stage. It appears that this may be a life time commitment for some, while it is possible that after your body has adjusted to a new metabolic process, you may be able to increase your carbohydrates slightly.
Although this is all speculation, I would imagine that once you have achieved your ideal weight loss, then you should increase the grams of carbohydrate until you maintain your weight. If you find that you are once again increasing in weight, this may reflect the necessity to either cut down the carbohydrates again and perhaps maintaining the appropriate amount of grams.
As with all things, there are for’s and against a low carbohydrate diet, although I can understand the suggested issues in regards to a restricted low carbohydrate diet, I feel we need to separate the normal form the abnormal and remember that we are not advocating a carbohydrate free diet, or a low carbohydrate diet for the average normal person who’s body is functioning well and absorbing glucose appropriately. Here we are primarily looking at the possibility of Hyperinsulinemia and management there-of.
Hyperinsulinemia has a major impact on your health due to the inability of weight loss. Example: If the average or normal person was to eat 2500 calories a day and work off 2600 calories which would leave them in a negative calorific state, they would lose weight even if the calories where from high carbohydrate and high fat. With Hyperinsulinemia, unless the calories were low fat and low carbohydrate, many would not lose weight, so if they kept the 2500 calories as pasta (carbohydrate) and a cream sauce for the topping (high fat) they actually wouldn’t lose weight despite being in a negative calorific state. Their weight would be more likely to remain the same where-as a normal individual would still lose weight as the carbohydrate metabolism wouldn’t be a problem.
Hyperinsulinemia IS A SERIOUS HEALTH ISSUE THAT NEEDS INVESTIGATING THOROUGHLY.
What Is Metabolic Syndrome?
Metabolic syndrome is the name for a group of risk factors that raises your risk for heart disease and other health problems, such as diabetes and stroke.
The term “metabolic” refers to the biochemical processes involved in the body’s normal functioning. Risk factors are traits, conditions, or habits that increase your chance of developing a disease.
In this article, “heart disease” refers to coronary heart disease (CHD). CHD is a condition in which a waxy substance called plaque builds up inside the coronary (heart) arteries.
Plaque hardens and narrows the arteries, reducing blood flow to your heart muscle. This can lead to chest pain, a heart attack, heart damage, or even death.
Metabolic Risk Factors
The five conditions described below are metabolic risk factors. You can have any one of these risk factors by itself, but they tend to occur together. You must have at least three metabolic risk factors to be diagnosed with metabolic syndrome.
- A large waistline. This also is called abdominal obesity or “having an apple shape.” Excess fat in the stomach area is a greater risk factor for heart disease than excess fat in other parts of the body, such as on the hips.
- A high triglyceride level (or you’re on medicine to treat high triglycerides). Triglycerides are a type of fat found in the blood.
- A low HDL cholesterol level (or you’re on medicine to treat low HDL cholesterol). HDL sometimes is called “good” cholesterol. This is because it helps remove cholesterol from your arteries. A low HDL cholesterol level raises your risk for heart disease.
- High blood pressure (or you’re on medicine to treat high blood pressure). Blood pressure is the force of blood pushing against the walls of your arteries as your heart pumps blood. If this pressure rises and stays high over time, it can damage your heart and lead to plaque build-up.
- High fasting blood sugar (or you’re on medicine to treat high blood sugar). Mildly high blood sugar may be an early sign of diabetes.
Your risk for heart disease, diabetes, and stroke increases with the number of metabolic risk factors you have. The risk of having metabolic syndrome is closely linked to overweight and obesity and a lack of physical activity.
Insulin resistance also may increase your risk for metabolic syndrome. Insulin resistance is a condition in which the body can’t use its insulin properly. Insulin is a hormone that helps move blood sugar into cells where it’s used for energy. Insulin resistance can lead to high blood sugar levels, and it’s closely linked to overweight and obesity. Genetics (ethnicity and family history) and older age are other factors that may play a role in causing metabolic syndrome.
Metabolic syndrome is becoming more common due to a rise in obesity rates among adults. In the future, metabolic syndrome may overtake smoking as the leading risk factor for heart disease.
It is possible to prevent or delay metabolic syndrome, mainly with lifestyle changes. A healthy lifestyle is a lifelong commitment. Successfully controlling metabolic syndrome requires long-term effort and teamwork with your health care providers.
What Causes Metabolic Syndrome?
Metabolic syndrome has several causes that act together. You can control some of the causes, such as overweight and obesity, an inactive lifestyle, and insulin resistance.
You can’t control other factors that may play a role in causing metabolic syndrome, such as growing older. Your risk for metabolic syndrome increases with age.
You also can’t control genetics (ethnicity and family history), which may play a role in causing the condition. For example, genetics can increase your risk for insulin resistance, which can lead to metabolic syndrome.
People who have metabolic syndrome often have two other conditions: excessive blood clotting and constant, low-grade inflammation throughout the body. Researchers don’t know whether these conditions cause metabolic syndrome or worsen it.
Researchers continue to study conditions that may play a role in metabolic syndrome, such as:
- A fatty liver (excess triglycerides and other fats in the liver)
- Polycystic ovarian syndrome (a tendency to develop cysts on the ovaries)
- Breathing problems during sleep (such as sleep apnea)
Who Is at Risk for Metabolic Syndrome?
People at greatest risk for metabolic syndrome have these underlying causes:
- Abdominal obesity (a large waistline)
- An inactive lifestyle
- Insulin resistance
- Some people are at risk for metabolic syndrome because they take medicines that cause weight gain or changes in blood pressure, blood cholesterol, and blood sugar levels. These medicines most often are used to treat inflammation, allergies, HIV, and depression and other types of mental illness.
Some racial and ethnic groups in the United States are at higher risk for metabolic syndrome than others. Mexican Americans have the highest rate of metabolic syndrome, followed by whites and blacks.
Other groups at increased risk for metabolic syndrome include:
- People who have a personal history of diabetes
- People who have a sibling or parent who has diabetes
- Women when compared with men
- Women who have a personal history of polycystic ovarian syndrome (a tendency to develop cysts on the ovaries)
- Heart Disease Risk
Metabolic syndrome increases your risk for coronary heart disease. Other risk factors, besides metabolic syndrome, also increase your risk for heart disease. For example, a high LDL (“bad”) cholesterol level and smoking are major risk factors for heart disease. For details about all of the risk factors for heart disease, go to the Coronary Heart Disease Risk Factors Health Topic.
Even if you don’t have metabolic syndrome, you should find out your short-term risk for heart disease. The National Cholesterol Education Program (NCEP) divides short-term heart disease risk into four categories. Your risk category depends on which risk factors you have and how many you have.
Your risk factors are used to calculate your 10-year risk of developing heart disease. The NCEP has an online calculator that you can use to estimate your 10-year risk of having a heart attack.
High risk: You’re in this category if you already have heart disease or diabetes, or if your 10-year risk score is more than 20 percent.
Moderately high risk: You’re in this category if you have two or more risk factors and your 10-year risk score is 10 percent to 20 percent.
Moderate risk: You’re in this category if you have two or more risk factors and your 10-year risk score is less than 10 percent.
Lower risk: You’re in this category if you have zero or one risk factor.
How Is Metabolic Syndrome Diagnosed?
Your doctor will diagnose metabolic syndrome based on the results of a physical exam and blood tests. You must have at least three of the five metabolic risk factors to be diagnosed with metabolic syndrome.
Metabolic Risk Factors
- A Large Waistline
Having a large waistline means that you carry excess weight around your waist (abdominal obesity). This is also called having an “apple-shaped” figure. Your doctor will measure your waist to find out whether you have a large waistline.
A waist measurement of 35 inches or more for women or 40 inches or more for men is a metabolic risk factor. A large waistline means you’re at increased risk for heart disease and other health problems.
- A High Triglyceride Level
Triglycerides are a type of fat found in the blood. A triglyceride level of 150 mg/dL or higher (or being on medicine to treat high triglycerides) is a metabolic risk factor. (The mg/dL is milligrams per deciliter—the units used to measure triglycerides, cholesterol, and blood sugar.)
- A Low HDL Cholesterol Level
HDL cholesterol sometimes is called “good” cholesterol. This is because it helps remove cholesterol from your arteries.
An HDL cholesterol level of less than 50 mg/dL for women and less than 40 mg/dL for men (or being on medicine to treat low HDL cholesterol) is a metabolic risk factor.
- High Blood Pressure
A blood pressure of 130/85 mmHg or higher (or being on medicine to treat high blood pressure) is a metabolic risk factor. (The mmHg is millimeters of mercury—the units used to measure blood pressure.)
If only one of your two blood pressure numbers is high, you’re still at risk for metabolic syndrome.
- High Fasting Blood Sugar
A normal fasting blood sugar level is less than 100 mg/dL. A fasting blood sugar level between 100–125 mg/dL is considered prediabetes. A fasting blood sugar level of 126 mg/dL or higher is considered diabetes.
A fasting blood sugar level of 100 mg/dL or higher (or being on medicine to treat high blood sugar) is a metabolic risk factor.
About 85 percent of people who have type 2 diabetes—the most common type of diabetes—also have metabolic syndrome. These people have a much higher risk for heart disease than the 15 percent of people who have type 2 diabetes without metabolic syndrome.
Retaining Water - Why Does it Happen?
What Is “Retaining Water” and Why does it Happen?
When you’re “retaining water,” what that actually means is that extra water is hanging around in the tissue between your cells. There are all kinds of reasons why this could possibly happen…
Diet: Carbohydrates and Salt
Carbohydrates and salt both cause water retention. This is why some people wake up the day after a non-Paleo meal and find that the scale has gone up 5 pounds. It is not 5 pounds of fat – that’s biologically impossible. But non-Paleo food is generally more carb-dense and saltier than Paleo food, and when you add the weight of that food in your stomach to the weight of retained water thanks to the extra carbs and salt, the total could very well be 5 pounds.
Want some numbers? Let’s start with the carbs. Every 1 gram of carbohydrate requires 3-4 grams of water to process and store it. To translate that into more familiar language, say you eat 1 medium Russet potato. You’ll be eating 37 grams of carbohydrate, which would require 111-148 grams of water. That’s 4-5 ounces, just under half a pound. On a moderate-carb diet, the average person will be retaining around 1.5 pounds of water weight just from carbs on a regular basis. If you go on a fast or simply stop eating all carbohydrates, you’ll lose that 1.5 pounds immediately.
You did not gain 5 pounds of fat from one unhealthy meal. But you may have gained 5 pounds of water.
Now imagine that you had a non-Paleo meal and ate a big plate of pasta (say, 3 cups of cooked pasta, which is normal for a place like Olive Garden) and a slice of chocolate cake for dessert. That’s 129 grams of carbs for the pasta, and around 72 grams for the cake – 201 grams of carbohydrate in total, which requires 603-804 grams of water. You just gained an extra 1.3-1.7 pounds of water weight from the carbohydrates in one meal, but that doesn’t mean you gained any fat. It’ll be gone in a few days.
With salt, it depends on how much you’re used to eating. Water retention from salt is driven by deviations from your “normal,” more than the absolute amount of salt consumed. In this study, men were put on four different diets; low-salt, normal-salt, high-salt, and then low-salt again. The men gained about 1 kilogram (2.2 pounds) from the low-salt to the normal-salt week, and an additional 0.5 kilogram (1.1 pounds) from normal-salt to high-salt.
Unfortunately, the study didn’t look at a single high-salt meal in the context of a low-normal salt diet, which is a more typical situation for people trying to lose weight, but it’s clear that healthy men can gain at least 2-3 pounds of water from increasing salt intake from low to high levels. For healthy women, the number is probably a little bit lower, just because women are smaller in general and have less tissue space to store the water in.
In any case, when you add up the carb weight and the water weight, plus the weight of an unusual amount of food in your stomach, you could easily “gain” 5 pounds from one meal without gaining any fat.
Sex Hormones (Especially for Women)
For women, the water-retention picture gets even more complicated. Most women know intuitively that they retain water at certain points in their cycle. In general (bearing in mind that everyone is different), 92% of women experience some water retention in week before their period starts. The amount of weight gained varies widely, but it’s typically around 5-10 pounds. Once menstrual bleeding actually begins, the water weight drops off again (although this isn’t always immediately obvious since many women feel bloated or uncomfortable from cramps, so the feeling of “puffiness” can persist).
Pregnancy and hormonal birth control can also affect water retention. Pregnancy usually causes women to retain more water, while hormonal contraceptives are a mixed bag.
This is very frustrating because most women are already physically smaller than men, and under stronger pressure to be consistently thin, so they’re more sensitive to fluctuations in their weight. Unfortunately, there’s not much anyone can really do about it, short of stopping a form of birth control if it drives you crazy.
Cortisol isn’t a demon hormone, but chronically elevated cortisol is a problem for many reasons, water retention among them. It’s hard to quantify specifically how much water retention cortisol can cause, because it can also increase fat gain so “cortisol weight” is probably a combination of both water and fat. But if you’re stressed and feeling bloated or puffy, at least some of that is likely to be water.
All kinds of things can raise cortisol levels, including calorie restriction and strenuous exercise – the exact behaviors that most people turn to for weight loss. Sleep deprivation or psychological stress will also do the trick.
Managing Water Retention
If you add up all those potential causes of water retention, you could easily get 10 pounds of weight fluctuation from water alone, and potentially more for premenstrual women or anyone who just suddenly ate a high-carb meal.
The #1 strategy for managing water retention without losing your mind: make peace with the fact that it’s just going to happen sometimes and there’s not much you can do about it. We might like to be able to control our weight down to the ounce, but in reality, that’s not how human bodies work. Ironically, stressing about it might just make you gain even more water weight from the cortisol.
But with that said, retaining water can sometimes be uncomfortable (if it’s extreme, especially in PMS) and there’s no point making those fluctuations bigger than they have to be.
So here are some tips for managing water retention:
- Exercise regularly. In the short term, intense exercise causes your muscles to retain water as part of the way they repair themselves. If you’ve ever felt your legs after a hard squat workout and noticed they felt swollen, they were – it’s because the workout caused you to retain water in those muscles. In the long-term, though, exercise helps prevent water retention by stimulating the flow of blood and lymphatic fluids that help remove water from the extremities.
Avoid huge variations in salt intake – pick a level that works for you and stick to it.
- If you’ve been dieting for a while, try a re-feed. In the Minnesota Starvation Experiment, many of the men retained water as a symptom of starvation, specifically “swollen legs, ankles, and faces.” When they increased their calories slightly, the water weight dropped off.
- As for supplements, this study found that magnesium reduced premenstrual water retention, but only if women kept it up for at least two months: there wasn’t a benefit the first month, but by the second month there was an effect. This study also found that magnesium and Vitamin B6 were helpful.
Summing it Up
Water retention can have a huge effect on your weight. If your cortisol is high and you find a stress reliever in a big high-carb, high-salt meal, it’s plausible that you could gain several pounds of water just from that. Most premenopausal women will naturally fluctuate several pounds up and down over the course of a month regardless of how much fat tissue they’re carrying.
Water weight can hide your weight-loss progress temporarily, but that doesn’t mean you’ve stalled. If you’re losing at a moderate but sustainable pace of 1-2 pounds a week, water weight fluctuations could even disguise a couple weeks of steady losses – it’s not the end of the world, and you won’t remember it in a year. Just keep on doing what works for you, and look forward to the “whoosh” when it drops off.
Original Source for: Water Weight
Obesity, Diet and Depression
Obesity and Depression May Be Linked
A major review reveals that research indicates people who are obese may be more likely to become depressed, and people who are depressed may be more likely to become obese.
To understand the potential links between obesity and depression, researchers led by Sarah M. Markowitz, M.S., examined the correlational data that suggest a connection between the conditions and found evidence for causal pathways from obesity to depression and depression to obesity.
People who are obese may be more likely to become depressed because they experience themselves as in poor health and are dissatisfied with their appearance. This occurrence was particularly prevalent among women and those of high socio-economic status.
People who are depressed may be more likely to become obese because of physiological changes in their hormone and immune systems that occur in depression. Also, they have more difficulty taking good care of themselves because of symptoms and consequences of depression, such as difficulty adhering to fitness regiments, overeating, and having negative thoughts.
Treatments such as exercise and stress reduction can help to manage both obesity and depression at the same time. Potentially, dieting, which can worsen mood, and antidepressants, which can cause weight gain, should be minimized.
“The treatment of depression and obesity should be integrated,” the authors conclude. “This way, healthcare providers are working together to treat both conditions, rather than each in isolation.”
This study is published in the March 2008 issue of Clinical Psychology: Science and Practice – Science Daily
Carbohydrates & Serotonin
Carbohydrates can affect levels of serotonin, but only indirectly. Eating carbohydrates together with protein-rich foods may boost the amount of tryptophan in your brain; tryptophan is then converted into serotonin.
However, there are no guarantees that you will change levels of serotonin by simply adjusting your carb intake. Other nutritional variables, as well as factors unrelated to your diet, such as sleep and exercise, also influence serotonin production.
As a neurotransmitter, serotonin carries signals between nerves. In the brain, serotonin regulates mood, pain perception, hunger and sleep cycles. It’s also active in your gut, but carbohydrates only affect serotonin in your brain. A structure called the blood-brain barrier determines which substances in the bloodstream get through to your brain. Since the barrier blocks serotonin, it must be synthesized inside the brain from an amino acid called tryptophan.
Tryptophan is an essential amino acid, so it must be obtained through your diet. After it’s consumed, tryptophan gains access to your brain through a transport system built into the blood-brain barrier. However, it competes with other amino acids to access the same transport structures. Tryptophan is outnumbered because foods contain a larger proportion of other amino acids, so its chances of getting into your brain are low. The best sources of tryptophan are poultry, fish, meat, milk and dairy products, eggs, soy products and nuts.
Impact of Carbohydrates
When you consume sugars and starches, your pancreas releases insulin, which is responsible for transporting sugar from your bloodstream into cells. Insulin also lowers the amount of amino acids in your blood except for tryptophan, which avoids insulin’s influence because it tends to bind with the protein albumin. As a result, the concentration of tryptophan increases and more transports across the blood-brain barrier.
While carbs increase the levels of tryptophan in your brain, and higher levels of tryptophan result in more serotonin, simply adding carbs does not guarantee you’ll increase serotonin levels. Some complex carbs, such as brown rice and beans, are also good sources of protein, and serotonin synthesis goes down when you consume large amounts of amino acids, according to the “Encyclopaedia of Neuroscience.” While simple carbs such as processed white bread and baked goods will trigger insulin without adding much protein, fresh fruits offer a healthier alternative – Healthy Eating
So depression isn’t just about low self-esteem because of obesity, nor is it just about becoming obese from over eating or poor eating habits because of depression.
Depression is not always due to life circumstances, or even because of how we think or feel about ourselves. Sometimes depression is due to dietary needs. This depression often appears to present itself differently to what is called clinical depression. In Dietary Depression (DD), it appears that one can not quite place a finger on the problem, it isn’t financial, it isn’t grief, it isn’t loss, it isn’t self-image, yet on initial questioning, it can appear to be any of the above or an accumulation of the above; but on further investigation, it is then realized that none of the above are the causes, they simply have exaggerated affects due to Dietary Depression. Dietary Depression can still feel like a heavy blanket over life, it can bring feelings of irritability, anger, fragility, emotional numbness and at times tearfulness. Dietary Depression can come on very suddenly, and go very suddenly, literally in days. One can get up tomorrow and feel either way; it can be described as similar to SAD’s (Seasonal Affective Disorder) but without as much emotions, where-as SAD’s can bring emotional (tearful) days, Dietary Depression appears to bring less emotions in way of tears but a mixed bag of emotions.
The underlying principle appears to be that in some cases, no matter what the instigator of depression is, the end result is in low serotonin levels. Carbohydrates are said to play an important role in the production chain of Serotonin as are proteins.
If you have Hyperinsulinemea; we already know that carbohydrates are an issue that perpetuates the Hyperinsulinemic cycle, so loading up on carbohydrates is not the answer but finding a balance is. If your body can mange fresh carbohydrates, as in those that come in fruits and vegetables, and you can have an adequate intake of protein, you should be able to maintain your serotonin levels, but if you cannot manage carbohydrates per saè, and you are not having sufficient protein, you are at possible risk of becoming low in Serotonin and affectively having some feelings of, or levels of Dietary Depression.
If you can recognize this in a positive way, in other words by becoming mindful of body mind and spirit, it will help you to understand what is going on inside your body and mind and assist you to deal with the issue positively and affectively at the onset without necessarily requiring anti-depressants which can cause so much weight gain.
If you require a natural supplement to boost your protein and serotonin levels, there are two products which I recommend, I do not get any type of re-imbursement for recommending them or from you purchasing them, I simply recommend them because I have found they have worked for many people.
Both products can be purchased from Solgar. There are cheaper versions available, but I feel and trust that Solgar products are of a high quality and often prove to be more affective. If I was going to purchase either of these products I would purchase them from this company.
Always Consult Your Doctor
Increasing Serotonin without Drugs
How to Increase Serotonin in the Human Brain without Drugs
Simon N. Young
For the last 4 decades, the question of how to manipulate the serotonergic system with drugs has been an important area of research in biological psychiatry, and this research has led to advances in the treatment of depression. Research on the association between various polymorphisms and depression supports the idea that serotonin plays a role, not only in the treatment of depression but also in susceptibility to depression and suicide.
The research focus here has been on polymorphisms of the serotonin transporter, but other serotonin-related genes may also be involved.1–5 In the future, genetic research will make it possible to predict with increasing accuracy who is susceptible to depression. Much less attention has been given to how this information will be used for the benefit of individuals with a serotonin-related susceptibility to depression, and little evidence exists concerning strategies to prevent depression in those with such a susceptibility. Various studies have looked at early intervention in those with prodromal symptoms as well as at population strategies for preventing depression.6–11 Obviously, prevention is preferable to early intervention; moreover, although population strategies are important, they are ideally supplemented with preventive interventions that can be used over long periods of time in targeted individuals who do not yet exhibit even nonclinical symptoms. Clearly, pharmacologic approaches are not appropriate, and given the evidence for serotonin’s role in the etiology and treatment of depression, nonpharmacologic methods of increasing serotonin are potential candidates to test for their ability to prevent depression.
Another reason for pursuing nonpharmacologic methods of increasing serotonin arises from the increasing recognition that happiness and well-being are important, both as factors protecting against mental and physical disorders and in their own right.12–14 Conversely, negative moods are associated with negative outcomes. For example, the negative mood hostility is a risk factor for many disorders. For the sake of brevity, hostility is discussed here mainly in relation to one of the biggest sources of mortality, coronary heart disease (CHD). A meta-analysis of 45 studies demonstrated that hostility is a risk factor for CHD and for all-cause mortality.15 More recent research confirms this. Hostility is associated not only with the development of CHD but also with poorer survival in coronary artery disease (CAD) patients.16 Hostility may lead to decreased social support and social isolation,17 and low perceived social support is associated with greater mortality in those with CAD.18 Effects are not just limited to CHD. For example, the opposite of hostility, agreeableness, was a significant protective factor against mortality in a sample of older, frail participants.19
The constitution of the WHO states “Health is a state of complete physical, mental and social well-being and not merely the absence of disease or infirmity.”20 This may sound exaggerated but positive mood within the normal range is an important predictor of health and longevity. In a classic study, those in the lowest quartile for positive emotions, rated from autobiographies written at a mean age of 22 years, died on average 10 years earlier than those in the highest quartile.21 Even taking into account possible confounders, other studies “found the same solid link between feeling good and living longer.”12 In a series of recent studies, negative emotions were associated with increased disability due to mental and physical disorders,22 increased incidence of depression,23 increased suicide24 and increased mortality25 up to 2 decades later. Positive emotions protected against these outcomes. A recent review including meta-analyses assessed cross-sectional, longitudinal and experimental studies and concluded that happiness is associated with and precedes numerous successful outcomes.26 Mood may influence social behaviour, and social support is one of the most studied psychosocial factors in relation to health and disease.27 Low social support is associated with higher levels of stress, depression, dysthymia and posttraumatic stress disorder and with increased morbidity and mortality from a host of medical illnesses.27
Research confirms what might be intuitively expected, that positive emotions and agreeableness foster congenial relationships with others.28,29 This in turn will create the conditions for an increase in social support.
Several studies found an association between measures related to serotonin and mood in the normal range. Lower platelet serotonin2 receptor function was associated with lower mood in one study,30 whereas better mood was associated with higher blood serotonin levels in another.31 Two studies found that greater prolactin release in response to fenfluramine was associated with more positive mood.32,33 The idea that these associations indicate a causal association between serotonin function and mood within the normal range is consistent with a study demonstrating that, in healthy people with high trait irritability, tryptophan, relative to placebo, decreased quarrelsome behaviours, increased agreeable behaviours and improved mood.34 Serotonin may be associated with physical health as well as mood. In otherwise healthy individuals, a low prolactin response to the serotonin-releasing drug fenfluramine was associated with the metabolic syndrome, a risk factor for heart disease,35 suggesting that low serotonin may predispose healthy individuals to suboptimal physical as well as mental functioning.
Nonpharmacologic methods of raising brain serotonin may not only improve mood and social functioning of healthy people — a worthwhile objective even without additional considerations — but would also make it possible to test the idea that increases in brain serotonin may help protect against the onset of various mental and physical disorders. Four strategies that are worth further investigation are discussed below.
The article by Perreau-Linck and colleagues36 (page 430 of this issue) provides an initial lead about one possible strategy for raising brain serotonin.
Using positron emission tomography, they obtained a measure of serotonin synthesis in the brains of healthy participants who underwent positive, negative and neutral mood inductions. Reported levels of happiness were positively correlated and reported levels of sadness were negatively correlated with serotonin synthesis in the right anterior cingulate cortex. The idea that alterations in thought, either self-induced or due to psychotherapy, can alter brain metabolism is not new. Numerous studies have demonstrated changes in blood flow in such circumstances. However, reports related to specific transmitters are much less common. In one recent study, meditation was reported to increase release of dopamine.37 The study by Perreau-Linck and colleagues36 is the first to report that self-induced changes in mood can influence serotonin synthesis. This raises the possibility that the interaction between serotonin synthesis and mood may be 2-way, with serotonin influencing mood and mood influencing serotonin. Obviously, more work is needed to answer questions in this area. For example, is the improvement in mood associated with psychotherapy accompanied by increases in serotonin synthesis? If more precise information is obtained about the mental states that increase serotonin synthesis, will this help to enhance therapy techniques?
Exposure to bright light is a second possible approach to increasing serotonin without drugs. Bright light is, of course, a standard treatment for seasonal depression, but a few studies also suggest that it is an effective treatment for nonseasonal depression38 and also reduces depressed mood in women with premenstrual dysphoric disorder39 and in pregnant women suffering from depression.40 The evidence relating these effects to serotonin is indirect. In human postmortem brain, serotonin levels are higher in those who died in summer than in those who died in winter.41 A similar conclusion came from a study on healthy volunteers, in which serotonin synthesis was assessed by measurements of the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) in the venous outflow from the brain.42 There was also a positive correlation between serotonin synthesis and the hours of sunlight on the day the measurements were made, independent of season. In rats, serotonin is highest during the light part of the light–dark cycle, and this state is driven by the photic cycle rather than the circadian rhythm.43,44 The existence of a retinoraphe tract may help explain why, in experimental animals, neuronal firing rates, c-fos expression and the serotonin content in the raphe nuclei are responsive to retinal light exposure.44–48 In humans, there is certainly an interaction between bright light and the serotonin system. The mood-lowering effect of acute tryptophan depletion in healthy women is completely blocked by carrying out the study in bright light (3000 lux) instead of dim light.49
Relatively few generations ago, most of the world population was involved in agriculture and was outdoors for much of the day. This would have resulted in high levels of bright light exposure even in winter. Even on a cloudy day, the light outside can be greater than 1000 lux, a level never normally achieved indoors. In a recent study carried out at around latitude 45° N, daily exposure to light greater than 1000 lux averaged about 30 minutes in winter and only about 90 minutes in summer50 among people working at least 30 hours weekly; weekends were included. In this group, summer bright light exposure was probably considerably less than the winter exposure of our agricultural ancestors. We may be living in a bright light–deprived society. A large literature that is beyond the scope of this editorial exists on the beneficial effect of bright light exposure in healthy individuals. Lamps designed for the treatment of seasonal affective disorder, which provide more lux than is ever achieved by normal indoor lighting, are readily available, although incorporating their use into a daily routine may be a challenge for some.
However, other strategies, both personal and institutional, exist. “Light cafes” pioneered in Scandinavia have come to the United Kingdom,51 and an Austrian village that receives no sunshine in the winter because of its surrounding mountains is building a series of giant mirrors to reflect sunlight into the valley.52 Better use of daylight in buildings is an issue that architects are increasingly aware of. Working indoors does not have to be associated with suboptimal exposure to bright light.
A third strategy that may raise brain serotonin is exercise. A comprehensive review of the relation between exercise and mood concluded that antidepressant and anxiolytic effects have been clearly demonstrated.53 In the United Kingdom the National Institute for Health and Clinical Excellence, which works on behalf of the National Health Service and makes recommendations on treatments according to the best available evidence, has published a guide on the treatment of depression.54 The guide recommends treating mild clinical depression with various strategies, including exercise rather than antidepressants, because the risk–benefit ratio is poor for antidepressant use in patients with mild depression. Exercise improves mood in subclinical populations as well as in patients. The most consistent effect is seen when regular exercisers undertake aerobic exercise at a level with which they are familiar.53 However, some skepticism remains about the antidepressant effect of exercise, and the National Institute of Mental Health in the United States is currently funding a clinical trial of the antidepressant effect of exercise that is designed to overcome sources of potential bias and threats to internal and external validity that have limited previous research.55
Several lines of research suggest that exercise increases brain serotonin function in the human brain. Post and colleagues56 measured biogenic amine metabolites in cerebrospinal fluid (CSF) of patients with depression before and after they increased their physical activity to simulate mania. Physical activity increased 5-HIAA, but it is not clear that this was due to increased serotonin turnover or to mixing of CSF from higher regions, which contain higher levels of 5-HIAA, with lumbar CSF (or to a combination of both mechanisms). Nonetheless, this finding stimulated many animal studies on the effects of exercise. For example, Chaouloff and colleagues57 showed that exercise increased tryptophan and 5-HIAA in rat ventricles. More recent studies using intracerebral dialysis have shown that exercise increases extracellular serotonin and 5-HIAA in various brain areas, including the hippocampus and cortex (for example, see58–60). Two different mechanisms may be involved in this effect. As reviewed by Jacobs and Fornal,61 motor activity increases the firing rates of serotonin neurons, and this results in increased release and synthesis of serotonin.62 In addition, there is an increase in the brain of the serotonin precursor tryptophan that persists after exercise.63
The largest body of work in humans looking at the effect of exercise on tryptophan availability to the brain is concerned with the hypothesis that fatigue during exercise is associated with elevated brain tryptophan and serotonin synthesis. A large body of evidence supports the idea that exercise, including exercise to fatigue, is associated with an increase in plasma tryptophan and a decrease in the plasma level of the branched chain amino acids (BCAAs) leucine, isoleucine and valine (see64,65 for reviews). The BCAAs inhibit tryptophan transport into the brain.66 Because of the increase in plasma tryptophan and decrease in BCAA, there is a substantial increase in tryptophan availability to the brain. Tryptophan is an effective mild hypnotic,67 a fact that stimulated the hypothesis that it may be involved in fatigue. A full discussion of this topic is not within the scope of this editorial; however, it is notable that several clinical trials of BCAA investigated whether it was possible to counter fatigue by lowering brain tryptophan, with results that provided little support for the hypothesis. Further, exercise results in an increase in the plasma ratio of tryptophan to the BCAAs before the onset of fatigue.64,65 The conclusion of these studies is that, in humans, a rise in precursor availability should increase serotonin synthesis during and after exercise and that this is not related to fatigue, although it may be related to improved mood. Whether motor activity increases the firing rate of serotonin neurons in humans, as in animals, is not known. However, it is clear that aerobic exercise can improve mood.
As with exposure to bright light, there has been a large change in the level of vigorous physical exercise experienced since humans were hunter-gatherers or engaged primarily in agriculture.68 Lambert68 argued that the decline in vigorous physical exercise and, in particular, in effort-based rewards may contribute to the high level of depression in today’s society. The effect of exercise on serotonin suggests that the exercise itself, not the rewards that stem from exercise, may be important. If trials of exercise to prevent depression are successful, then prevention of depression can be added to the numerous other benefits of exercise.
The fourth factor that could play a role in raising brain serotonin is diet.
According to some evidence, tryptophan, which increases brain serotonin in humans as in experimental animals,69 is an effective antidepressant in mild-to-moderate depression.67,70 Further, in healthy people with high trait irritability, it increases agreeableness, decreases quarrelsomeness and improves mood.34 However, whether tryptophan should be considered primarily as a drug or a dietary component is a matter of some dispute. In the United States, it is classified as a dietary component, but Canada and some European countries classify it as a drug. Treating tryptophan as a drug is reasonable because, first, there is normally no situation in which purified tryptophan is needed for dietary reasons, and second, purified tryptophan and foods containing tryptophan have different effects on brain serotonin.
Although purified tryptophan increases brain serotonin, foods containing tryptophan do not.71 This is because tryptophan is transported into the brain by a transport system that is active toward all the large neutral amino acids and tryptophan is the least abundant amino acid in protein. There is competition between the various amino acids for the transport system, so after the ingestion of a meal containing protein, the rise in the plasma level of the other large neutral amino acids will prevent the rise in plasma tryptophan from increasing brain tryptophan. The idea, common in popular culture, that a high-protein food such as turkey will raise brain tryptophan and serotonin is, unfortunately, false. Another popular myth that is widespread on the Internet is that bananas improve mood because of their serotonin content. Although it is true that bananas contain serotonin, it does not cross the blood–brain barrier.
α-Lactalbumin, a minor constituent of milk, is one protein that contains relatively more tryptophan than most proteins. Acute ingestion of α-lactalbumin by humans can improve mood and cognition in some circumstances, presumably owing to increased serotonin.72,73 Enhancing the tryptophan content of the diet chronically with α-lactalbumin is probably not practical. However, increasing the tryptophan content of the diet relative to that of the other amino acids is something that possibly occurred in the past and could occur again in the future. Kerem and colleagues74 studied the tryptophan content of both wild chickpeas and the domesticated chickpeas that were bred from them in the Near East in neolithic times. The mean protein content (per mg dry seed) was similar for 73 cultivars and 15 wild varieties. In the cultivated group, however, the tryptophan content was almost twice that of the wild seeds. Interestingly, the greater part of the increase was due to an increase in the free tryptophan content (i.e., not part of the protein).
In cultivated chickpeas, almost two-thirds of the tryptophan was in the free form. Kerem and colleagues74 argue that there was probably selection for seeds with a higher tryptophan content. This is plausible, given another example of an early strategy to increase the available tryptophan content of an important food source. Pellagra is a disorder caused by niacin deficiency, usually owing to poverty and a diet relying heavily on corn (maize), which has a low level of niacin and its precursor tryptophan. Cultures in the Americas that relied greatly on corn used alkali during its processing (e.g., boiling the corn in lime when making tortillas). This enhanced the nutritional quality of the corn by increasing the bioavailability of both niacin and tryptophan, a practice that prevented pellagra.75 The Europeans transported corn around the world but did not transport the traditional alkali-processing methods, thereby causing epidemics of pellagra in past centuries. Breeding corn with a higher tryptophan content was shown in the 1980s to prevent pellagra76; presumably, it also raised brain serotonin. In a recent issue of Nature Biotechnology, Morris and Sands77 argue that plant breeders should be focusing more on nutrition than on yield. They ask, “Could consumption of tryptophan-rich foods play a role in reducing the prevalence of depression and aggression in society?” Cross-national studies have reported a positive association between corn consumption and homicide rates78 and a negative association between dietary tryptophan and suicide rates.79 Although the idea behind such studies is interesting, any causal attribution must remain speculative, given the possible confounds. Nonetheless, the possibility that the mental health of a population could be improved by increasing the dietary intake of tryptophan relative to the dietary intake of other amino acids remains an interesting idea that should be explored.
The primary purpose of this editorial is to point out that pharmacologic strategies are not the only ones worthy of study when devising strategies to increase brain serotonin function. The effect of non-pharmacologic interventions on brain serotonin and the implications of increased serotonin for mood and behaviour need to be studied more. The amount of money and effort put into research on drugs that alter serotonin is very much greater than that put into non-pharmacologic methods. The magnitude of the discrepancy is probably neither in tune with the wishes of the public nor optimal for progress in the prevention and treatment of mental disorders.
Chromium, Blood Sugar, Carb Cravings and Body Fat
Chromium Helps Control Blood Sugar, Curbs Carb Cravings and Fights Body Fat
Stabilizing blood sugar is important for a healthy body weight
by Jeff S. Volek, Ph.D., R.D.
Chromium is an essential trace mineral that has received much attention as a dietary supplement because good dietary sources of chromium are scarce and intake is generally low. There is debate, however, regarding optimal amounts and exactly how chromium works in the body. In recent years, some very elegant work has revealed that chromium augments the actions of insulin, which is consistent with studies showing that long-term use effectively controls blood sugar (glucose) levels in people with intolerance to carbohydrates. Better control of blood sugar levels has several favorable effects.
When you eat carbohydrate, it is broken down to sugar and absorbed into the blood. The magnitude of the rise in blood sugar, and subsequent rise in insulin, varies widely from food to food. Slowing the release of sugar into the blood is the first step to controlling blood sugar and one of the most important goals of any healthy diet.
According to research, keeping blood sugar in check does everything from enhancing weight and fat loss and decreasing appetite to warding off several chronic diseases like heart disease, diabetes, etc. In contrast, foods that are rapidly digested and quickly released into the blood promote overeating, obesity, insulin resistance, and other metabolic disturbances contributing to disease.
Chromium helps control blood sugar
Chromium supplementation is a simple method to improve blood sugar control in some people. Several studies have evaluated the effect of chromium on glucose levels with varied results, but a significant number of these studies have shown that chromium can normalize blood sugar levels, improve blood sugar utilization and decrease insulin requirements in patients with glucose intolerance and insulin resistance. In one study, blood sugar responses to a carbohydrate meal of white bread were measured with and without a single dose (400 micrograms) of chromium. The addition of chromium resulted in a 23% reduction in blood sugar after the meal. Thus, taking chromium with carbohydrate-rich foods may be an effective way to lower the glycaemic index of that meal.
Chromium and cholesterol levels
Chromium also plays a role in fat metabolism. Several studies have investigated chromium’s effects on lipid profiles. A number of those studies reported reductions in triglycerides, as much as 32%, and reductions in total and LDL cholesterol. These positive effects were noted when studying the risk for heart disease in healthy people and those with diabetes or glucose intolerance.
Chromium diminishes carb cravings
If you are like a lot of people, you might have a compelling and recurring hunger for carbohydrate-rich foods. Cravings for starchy and sugar-laden foods are common and are a type of addiction that involves similar mechanisms engaged by opiates and the pain/pleasure center of the brain.
In one study, it was shown that simply taking 600 micrograms of chromium picolinate for 8 weeks significantly reduced carbohydrate cravings. The subjects who had the most severe carbohydrate cravings experienced the best results. When blood sugar is low, the drive to seek out sugars and starches is amplified, and there is a tendency to overconsume calories.
Although not addressed in this study, chromium supplementation may have helped to stabilize blood sugar levels and diminish the desire for carbohydrate-laden foods.
Chromium fights body fat
There have been fewer studies focused on chromium supplementation by athletes, but some double-blind, placebo-controlled experiments have shown that chromium picolinate supplementation reduces fat mass, increases lean body mass and can lead to weight loss. In one study, chromium picolinate was able to increase lean body mass in obese patients placed on a very low calorie diet.
Chromium combats insulin resistance
The exact role of chromium has eluded researchers, but recent evidence indicates that chromium plays an important role in insulin signaling. Poor insulin signaling, or insulin resistance, is a prevalent condition that contributes to obesity and several other metabolic problems that predispose people to diabetes and heart disease. Therefore, anything that combats insulin resistance (like exercise) is generally viewed as health-promoting.
One study examined the effects of chromium in rats that were obese and insulin resistant. The results clearly showed that rats given additional chromium in their drinking water significantly improved glucose disposal rates and insulin-stimulated signaling in skeletal muscle. In other words, extra chromium improved the insulin resistance normally present in these animals.
These findings are consistent with several studies showing improved glucose control in people with glucose intolerance and insulin resistance. Since glycogen synthesis and protein synthesis are regulated by insulin signaling, adding chromium could stimulate these processes in individuals who are insulin resistant.
My lab investigated the potential of chromium picolinate to improve glycogen synthesis after intense exercise in healthy men. Although chromium led to very high rates of glycogen synthesis during the recovery phase after exercise, the values were not significantly different than the placebo group.
However, we did find that chromium engaged a different cellular pathway in muscle that bypassed one of the steps often deficient in people with glucose intolerance and diabetes.
How much chromium to take
Chromium supplementation is safe with no reported significant side effects. Effective doses seem to be in the range of 200 to 600 micrograms (0.2 to 0.6 mg). It is typically sold in 200 microgram capsules or tablets.
There are several types of chromium supplements available, such as chromium chloride, chromium polynicotinate and chromium picolinate. Chromium picolinate is remarkably stable and remains intact for several hours in synthetic gastric juice. The comparative data results of chromium picolinate versus other forms of chromium demonstrated that it is the most effective form to facilitate glucose control. It was also observed that chromium picolinate is better absorbed physiologically (2.5%) than chromium chloride (0.5-1%) and chromium acetate (0.8%); chromium oxide is not absorbed at all (0.001%).
Article from: Nutrition Express
Body Mass Index (BMI)
Planking Your Core – Resistance Training for Core Strength
Resistance training causes the muscles to contract against an external resistance with the expectation of increases in strength, tone, mass and/or endurance. The external resistance can be dumbbells, your own body weight, or even bottles of water; in fact the external resistance can be any object that causes the muscles to contract, which means you don’t need expensive gym memberships or expensive equipment to build a strong core.
We need a strong core as it affects how we walk, how we stand and what we can accomplish physically in our average day; Yoga is another way to build a strong core.
If you are disabled, you may find that your core has always been, or has become weak over time, you may find that you are not able to ever complete the 5 Minute Workout or The Core Muscle Strength & Stability Test below: But you may be able to manage 30 seconds a day or 1 minute a day of Planking. Work with your body, your physical limitations and your physiotherapist if you have one, or any other health consultant that you have available and commit to as much as your limitations permit.
It will be hard when you start, but it will make a HUGE difference.
Many people will be unable to complete The Core Muscle Strength & Stability Test below. Many people are unable to hold any Plank position for more than 30 seconds so do not despair.
A good way to start Planking is to use the workout image below.
Start at the beginning and do NOT move on until you can hold the first position for a minute, when you can, then add in the second position and don’t move on until you can successfully manage the first two together. Then continue on in the same manner until you can do the full 5 Minute Workout.
When you can manage the full 5 Minute Workout, try to complete it once a day, this will give you a good strong core.
You will be surprized at how fast your ability to perform the Planks increase. When you can manage the 5 Minute Workout, complete The Core Muscle Strength & Stability Test
The Core Muscle Strength & Stability Test
The objective of this evaluation is to monitor the development and improvements of an athlete’s core strength and endurance over time.
To prepare for the assessment you will need:
Watch or clock with second counter
Conducting the Test
Position the watch or clock where you can easily see it
Start in the Plank Exercise Position (elbows on the ground) (second position in the image below)
Hold for 60 seconds
Lift your right arm off the ground (fourth position in the image below)
Hold for 15 seconds
Return your right arm to the ground and lift the left arm off the ground (as above)
Hold for 15 seconds
Return your left arm to the ground and lift the right leg off the ground (third position in the image below)
Hold for 15 seconds
Return your right leg to the ground and lift the left leg off the ground (as above)
Hold for 15 seconds
Lift your left leg and right arm off the ground (fourth position in the image below BUT with the leg raised)
Hold for 15 seconds
Return you left leg and right arm to the ground
Lift your right leg and left arm off the ground (as above)
Hold for 15 seconds
Return to the Plank Exercise Position (elbows on the ground)
Hold this position for 30 seconds
(3 minutes in total)
Good Core Strength
If you can complete the test fully, you have good core strength.
Poor Core Strength
If you can not complete the test fully, your core strength needs improvement.
Poor core strength results in unnecessary torso movement and swaying during all other athletic movements. This results in wasted energy and poor biomechanics. Good core strength indicates that the athlete can move with high efficiency.
If you are unable to complete the test practice the routine three or four times each week until you improve.
By comparing your results over time, you will note improvements or declines in core strength.
About the Test Design
Core Muscle Strength & Stability Test was designed by Brian Mackenzie , a senior athletics coach (UKA 4) with UK Athletics, the United Kingdom’s National Governing body for Track and Field Athletics.