Take some time to think about yourself

*****

Go back four or five years and I was on the traditional carb-heavy active person’s diet (porridge each morning, pasta salads and bakes for lunch, pasta and rice-laden meals at dinner).  I was living in my trainers, had lots of stress from day to day, plenty of cardio through walking and cycling, no weights, no supplements.  I couldn’t even overhead press an empty dumbbell handle weighing a hefty 1kg.  As for my body weight, I had weighed 50kg for about 10 years, despite being 5’6”, with it never going either up or down.

Sound familiar?

Since then I’ve been through a journey of discovery.

I’ve converted to an almost carb-free existence for a while to learn to be a fat-burner, I went strictly paleo for long enough that I can now get away with the odd non-Paleo diversion from time to time but know that I’m looking after my body the rest of the time.

I care for myself better, both mentally and physically.  I have learned to control my stress levels better and know how to recognise my stress characteristics and manage them.  I can feel different muscles in my body working with an awareness I never had before and, as a result I can use self-massage techniques to keep my body feeling as free and relaxed as possible.

Elsewhere in my life I’ve converted to living in Vibram KSOs whenever I can get away with them.  I still cycle and walk a huge amount but I balance it now with a programme of lifting weights.  I’m push-pressing a 20kg kettlebell for reps, squatting safely over my national qualifying weight (with the BDFPA) and happily hip thrust 140kg for reps.

As for my body composition, I’ve gained an enormous amount of muscle and struggle to keep my weight near 56kg because my love of food, when put alongside the hours I spend sitting still in my desk job mean that it tends to drift up a kilo or two at times, despite the fact that I’m carrying less body fat than I was when I weighed 50kg.  I definitely can’t fit my quads, hamstrings or glutes into any of the jeans I used to wear (which is actually a bit frustrating, but never mind).

*****

It’s a lot of changes in a surprisingly short space of time and that’s just what I’ve achieved without removing the full time desk job from my life.  I expect that a lot of others who read this blog have come through similar journeys of self-discovery and change in the recent past.

Have you adopted some changes to diet, training or lifestyle and seen similar massive changes and benefits to your overall being?

No related posts.

As with all games of word association, this game of links association is perhaps a bit tenuous in places with some dubious segues to get us from link to link but I was genuinely interested and surprised by some of the bits I’ve been putting aside and hope you will too.

We're even going to manage to find some links about sleep in here... is that how Jake stays lean?

• I’ve been intrigued by this review of Read my Hips by Kim Brittingham.  I think body image is a real issue for many women and it looks like this could be a fascinating look into someone’s battles with their self-image.
• Despite that comment on self-image I’m having a brief diet period.  My hips and thighs have got a bit out of control with the work lunches and dinners I’ve had recently and I feel uncomfortable in my clothes and skin now.  I don’t want to have to buy new clothes for only a couple of months in the office.  I know – it’s perhaps a bit hypocritical after a link to self-image.  Anyway, part of my “diet” involves plenty of sleep.  Especially now that I’ve seen reference to a study suggesting that those dieting and getting less sleep lose more of their weight as muscle loss and experience more hunger.
• Sleep is not just crucial for losing weight of the right type.  I was also interested to read that reduced sleep (four hours or less) can reduce insulin sensitivity.  Reduced insulin sensitivity is likely to impact on your weight management and your overall health.  By implication constantly missing sleep could lead to type 2 diabetes and other related conditions.  Though there’s a great suggestion in this article – intermittent fasting has been shown to improve insulin sensitivity so perhaps fast after a bad night of sleep (though personally I find I’m always ravenously hungry after a bad night).
• So picking up on the intermittent fasting theme in the previous link, the same site (Naturally Engineered) also had an article comparing calorie restriction and intermittent fasting, providing some nice simple explanations to squash the myth that the two are the same thing.  They might be – I certainly find that intermittent fasting can sometimes help with a highly calorie restricted diet since my one meal of the day feels like a sensible size – but it doesn’t have to be.
• Even if you don’t practice intermittent fasting on a regular basis like I do, Jamie Scott brought my attention to a study highlighted in Science Daily that suggests links between routine periodic fasting and improved general health (including heart health).  So even if you don’t need to fast to improve insulin sensitivity perhaps you might consider doing a fast every now and again anyway.
• Dietary fat has also been flagged by many people as providing some excellent health benefits so perhaps some fat in those meals would help?  Don at Primal Wisdom did a bit of a high-level meta-analysis of four studies looking at the effect of fat content on meal satiety.  After all, if you’re fasting you want to feel satiated before you start your fast.  I would have expected the overall conclusion to be that fat was much more satiating than carbohydrates so I was really surprised to see Don concluding that carbohydrates would be more satiating and that to replace carbs with fat and remain equally satiated would most likely involve a much higher calorie intake.  Not so good for weight loss!
• So we’re now thinking that perhaps we should eat more carbohydrate rather than fat when dieting to keep the calorie level down.  But are the carbohydrates good for our health?  Let’s turn to a study highlighted by Healthy Diets and Science, which I haven’t looked at in detail but the summary results seem to suggest that of the Italian women studied, those with the highest carbohydrate intake also had twice the risk of coronary heart disease.
• But wait!  Brian St Pierre spent two articles explaining why pointing the finger at carb misses the point.  In part two he uses the classic example of the Kitavans to show that there are populations who don’t have horrible health problems as a result of eating plenty of carbs in their diet.  To quote the article: “Dr. Lindeberg found that heart disease and stroke are absent or exceedingly rare in this population. They are completely unfamiliar with the signs and symptoms of heart attack and stroke, and the lack of these diseases was confirmed with their excellent ECG’s.”  So the lesson from this is perhaps that we should be careful of extrapolating one study on a specific population to all other populations.

So we started out at body image and dieting for our figures and ended up at the everlasting debate about whether carbohydrates are good or bad for us.  I wouldn’t have seen that one coming – certainly not taking the route I took on the way.

I’d love to know if you’ve enjoyed this game of links association and found some of the resulting links useful.  If you have I might do another one later this year on a different theme.

Related posts:

1. Blog-watch: diet and other health-related blogs
2. Blog-watch: paleo diet links
3. Blog-watch: pregnancy diet and exercise

Type 2 diabetes can be very easily and effectively managed with slight changes to lifestyle, diet or whatever the source is proposing and it can also, in most circumstances, be resolved permanently.  In fact, it seems that almost anything that takes you away from our modern junk-food, immobile and stressed lifestyle can contribute to improving type 2 diabetes.

Below is some information about the most compelling ways I’ve read about to improve and possibly even cure type 2 diabetes.

What is type 2 diabetes?

To kick off take a quick reminder read of my diabetes introductory post.  Diabetes is caused when the body can’t take control of elevated glucose levels and handle the glucose correctly, storing it appropriately for use as energy later on.

Unlike type 1 diabetes, where the body is unable to produce insulin that triggers the storage process for glucose, type 2 diabetics produce insulin but their bodies are unable to use the insulin correctly – they are insulin resistant.  As a result of this they still don’t process and store the glucose and the glucose is allowed to build up and flood the system.  Essentially, the insulin isn’t triggering those GLUT4 molecules in the cells, telling them to latch onto glucose and both turn it into a storable form and take it to the correct storage facilities (the liver and muscles).

If you didn’t read the introductory post that I wrote on diabetes and which I linked to in the first paragraph of this section then you might want to go and read it now to find out what happens to people when they get a long-term build-up of glucose in their blood.

Cause of type 2 diabetes

Knowing what causes type 2 diabetes is difficult to put your finger on.  While Wikipedia lists all sorts of causes of type 2 diabetes I disagree with the spirit of the list.  For me the reality is that it could most simply be summarised as “living the Western life”.  If you eat a western diet (plenty of grains, wheat, sugar and so on) and live the western lifestyle (stress, inactivity etc) then you are quite possibly storing up the possibility of becoming insulin resistant.

Grain-based foods like pasta - are they to blame?

Why is that?

The short answer is that your body will become insulin resistant when it is made to handle massively elevated glucose levels day-in, day-out, for weeks, months and years and the system is therefore flooded with insulin all the time.  It stops knowing how to respond to the insulin – it can’t be on high alert all the time.

Some western living conditions, such as stress, which are known to contribute to metabolic derangement, can cause the body to go into this state faster, but really we need to look at what is causing the body to be permanently flooding with insulin and the answer is found in the typical western diet which consists of not only the obvious culprit, sugar, but also contains plenty of wheat.

Excessive wheat consumption causes spikes in glucose and, correspondingly, spikes in insulin every time you consume it.  It has been shown to produce a “belly” on people (there’s your obesity cause of type 2 diabetes) and it has also been linked to metabolic syndrome and problems with testosterone levels, all of which are listed on Wikipedia as potential causes of type 2 diabetes.  In fact, wheat consumption is starting to be linked with a huge number of western diseases, many of which are in turn linked with diabetes.

So is there any actual evidence to directly link wheat consumption with diabetes?  Well, it might be circumstantial evidence, but Robert Paterson took some time to look at the percentage of the US population with diabetes and the pattern of wheat consumption over the years.  The results are very compelling and strongly implicate wheat consumption as one of the main causes of diabetes.

Of course you could decide to believe all the many other studies suggesting that foods like red meat cause type 2 diabetes, but these are generally observational studies where other dietary factors are poorly controlled or recorded.  To take that on the other side, you could similarly argue that Robert Paterson’s connection is purely assumption or coincidence and that something else is at work here.

You may also be from the camp that believes that high fat diets cause diabetes, but Robb Wolf  and Denise Minger very squarely put to bed any belief that the latest study showing this is reliable.  Not only did carbohydrate levels also increase notably in the experiment’s “high-fat diet” but Robb also brings the reader’s attention to a separate study with a high-fat ketogenic diet (low, cyclical carb intake) that showed benefits related to type 2 diabetes complications.

Curing type 2 diabetes

Based on the belief that the principle cause of type 2 diabetes is over-exposure to high glucose-creating carbohydrates such as sugar, grains and, more specifically, wheat, the basic cure should be removal of those foods from the diet.  At first this may only be a controlling measure and it may take years of keeping these out of the diet before a person’s body stops being flooded by insulin and learns to respond correctly to insulin when it does get the odd burst.  Over time the individual may completely recover so that they are no longer insulin resistant.

To support this it is worth considering the experience of Jeff O’Connell (author of Sugar Nation).  Jeff believes that while he had a genetic propensity for type 2 diabetes he was also the classic skinny-fat build, carrying more body fat than was immediately visible.  Jeff managed to get control over his diabetes by cutting out the refined carbohydrates in his diet and moving to a low carbohydrate diet.

Peter at Hyperlipid is also in agreement with this as a solution to type 2 diabetes.  In fact, it sounds very much like a low carbohydrate and/or a paleo diet could be the solution for many type 2 diabetics if you wanted to put a name on the diet.  Unsurprisingly, there’s even a study (D Klonoff: The Beneficial Effects of a Paleolithic Diet on Type 2 diabetes and other risk factors for cardiovascular disease.  J Diabetes Sci Technol. 2009; 3(6):1229-1232) supporting the paleo diet as a solution.

Oh, and we’re not the first to think of this either.  In The Starvation Treatment of Diabetes, some doctors record how they were very effectively treating and controlling diabetes with a low carbohydrate diet before 1916!

The problem with the medical practice – a brief rant

I get thoroughly frustrated by the modern medical establishment’s proposed diet for diabetics.  They generally prescribe regular intake of “healthy grains” such as oats, at a level that seems to be much higher than the successful levels documented in The Starvation Treatment of Diabetes, although on the plus side they do tell people to remove sugar from their diet.  The logic seems to be to keep the glucose levels in the blood level constant and avoid spikes of blood sugar that can’t be controlled.

This is not a cure, it’s a way to maintain the current diabetic status without it getting worse.  Unfortunately there is a general belief that humans must have carbohydrates to provide essential energy to live on a daily basis and so this diet for diabetics is finding a way to provide this carbohydrate intake without excessively fluctuating blood glucose levels and creating corresponding insulin spikes.

I’ve written before that this belief in carbohydrate being essential for day-to-day living is inaccurate.  Human’s need glucose as essential energy only to run the brain and for significant muscular efforts.  It’s not actually that big a requirement.  All other energy can come from fat and I therefore think it is really important for any type 2 diabetic to learn to effectively utilise fat as a fuel source so that they can remove their dependency on carbohydrates.

Other ways to improve type 2 diabetes

There are plenty of other ways to help improve type 2 diabetes, in particular through improving insulin sensitivity.  I’ve pulled together a couple of particularly well-recognised ideas below.

Exercise

Most people who practice resistance training (lifting weights) know that it is particularly good for increasing insulin sensitivity.  The reason for this is that the exercise uses up glycogen stores in the muscles and the body is subsequently attuned to want to process glycogen correctly and refill those stores straight after exercise.  Note that this is not “exercise” as a stroll around the block or a 5 minute jog on the treadmill, this is “exercise” as a serious muscle-fatiguing activity.

Shift some big weights to improve insulin resistance

Some really good reading on this subject comes from Charles Poliquin who explains in part one of a series on insulin resistance and body composition that large volume and high intensity work will be the most effective at improving insulin sensitivity.

Coincidentally, Charles also flags up in the same article a study linking decreased testosterone levels in men with increased incidence of type 2 diabetes.  Since heavy resistance training can increase testosterone levels (as can reducing wheat consumption, by the way) this puts a double-tick in the resistance training box.

Supplementation

Vitamin D is a bit of a wonder-vitamin.  It has been shown to improve all sorts of things, however Dr Briffa did a great article recently showcasing a systematic review of 8 different studies (Mitri J, et al. Vitamin D and type 2 diabetes: a systematic review. Eur J Clin Nutr. 2011 Jul 6. doi: 10.1038/ejcn.2011.118).  As Dr Briffa points out while the evidence from a single study of vitamin D (such as a study done by PR von Hurst and published in the British Journal of Nutrition in 2011) would be interesting there is always a risk that something other than the vitamin has caused the changes.  Once you bring together evidence from 8 studies then the link between high vitamin D levels and improved insulin sensitivity.

Vitamin D - all hail the great vitamin!

*****

I hope this is helpful to you all.  Hopefully it at least gives you some ideas of some potential avenues to try out if you are a type 2 diabetic or know someone who is.  In particular I really do strongly recommend reading the first part of The Starvation Treatment of Diabetes for anyone who tries to claim that they absolutely must follow the guidelines and eat numerous small meals with plenty of “healthy grains” each day.  Doctors were successfully treating diabetes through several days of starvation before slow increases in various foods except fat where the intake level makes up most of the caloric intake.

Related posts:

1. Type 1 diabetes
2. Type 1 diabetes: a possible cure
3. Diabetes: an introduction

• Stephan supports the hypothesis that obesity is caused by the palatability of food – if I’ve understood it correctly people eat more food if it is more palatable and therefore they become obese which in today’s age, when a huge number of foods are carefully processed and chemically enhanced to be appealing to people’s tastes, is why we have such a problem with obesity.
• Gary believes that the problem lies with carbohydrates and our consumption of certain types of carbohydrates in particular.

I am absolutely not going to get onto this bandwagon of debate.  Debate is what drives scientific and non-scientific discovery.  If we didn’t have people disagreeing with hypotheses and developing their own hypothesis before then carrying out research to see if their hypothesis is correct we would never progress and increase our understanding of how things really work.

In this case I think there is merit to both hypotheses and I suppose for me the issue is really one of where the obesity problem originates – which of these two issues is the initial driver of obesity?  However, it is a fascinating debate so I’ve pulled together this blog-watch of the debate so far for those who would like to follow it.

The hypotheses

For those who don’t know Gary’s theory here are three videos together making up an interview with Gary in which he explains his hypothesis:

http://www.youtube.com/watch?v=XR3FVvEJ-Nk

http://www.youtube.com/watch?v=myyOD1W1DPg

http://www.youtube.com/watch?v=4HxLeGvFVsM

For those who don’t know Stephan’s viewpoint you could do worse than start with his eight part series on Food Reward which you can find at the following links: one, two, three, four, five, six, seven, eight.  The last article contains links to plenty of further reading on this hypothesis of food reward and palatability.

The debate

Here’s a video of the debate between Gary Taubes and Stephan Guyenet at the end of Stephan’s presentation during the Ancestral Health Symposium:

http://www.youtube.com/watch?v=4hzoFgwFeMQ

So here are some posts and articles about the debate kicked off during that Q&A at Stephan’s presentation at the Ancestral Health Symposium.

• I’m going to start with Stephan writing about the debate at the Ancestral Health Symposium.
• Following that debate at the Q&A session, Stephan seemed to decide that the best approach was to do a critical examination of the carbohydrate theory of obesity.  This is Gary’s hypothesis.
• To compare with this so that it can be balanced by Gary’s view of the food palatability and overeating hypothesis, having checked out Gary’s blog it looks like he was thinking about food reward and overeating long before this debate.  A post written in December 2010 addressed his view of overeating and why he felt it was a nonsensical explanation for why we get fat.
• Moving on from each of their considerations of the hypothesis supported by the other person, Stephan then did an interesting article about food palatability and how this links in with the concept of the body having a set point for its weight.  Soon after this he did an article outlining his understanding of the factors promoting obesity in humans.  As you can imagine, there isn’t just one.
• Gary Taubes has decided to do a series addressing the debate.  The first post in the series was long and it seems that even then he was anticipating not getting onto Stephan’s hypothesis until part three!  Initially Stephan did a response to this post and it caused a huge amount of hot air in the blog-world, but he has since decided to withdraw his response and wait until Gary has completed his series before responding.
• A challenge had been put out to Stephan to test the theory of food palatability.  Off the back of this challenge Stephan did design a food reward study and starting asking for volunteers before being challenged about it by the University of Washington where I understand he works.  As a result of this Stephan has decided to cancel the study.
• Of course, while all of this is going on (and we’ll be a while yet before this is over) a few other people have weighed in with their views.  In particular, Peter at Hyperlipid has done a very technical article looking at the debate.  You’ll need your technical thinking caps on to work through his article though!

I can see this going on for some time so for those who are interested in this I recommend that you bookmark both Stephan’s blog, Whole Health Source, and Gary’s blog and watch as the debate continues.

Related posts:

1. Raw food
2. 15 Ways to Survive a Desk Job – Part 1 (food and drink)
3. Real experiences compared to hypotheses about the menstrual cycle

What is type 1 diabetes?

Type 1 diabetes is defined by the John Hopkins Medical Institutions website as “an inflammatory autoimmune disease of the pancreas, resulting in a lack of insulin” (1).  Without sufficient insulin, the body can’t store the free glucose in the blood, and blood glucose levels can rise unchecked.

Last week, while explaining the process of how our bodies deal with elevated blood glucose levels and what happens when this goes wrong, I made passing mention to beta cells.  These are cells found in the pancreas and are the cells which produce insulin.  In the case of a type 1 diabetic the body does not produce sufficient insulin because it has attacked and killed off most of the beta cells. 

In fact, the John Hopkins site notes that more than 90% of the beta cells will have been destroyed before the clinical symptoms of diabetes develop (1).  In effect, that tells us that by the time someone realises they have diabetes, they have already been developing diabetes for a long time.

How is type 1 diabetes diagnosed?

Classically diagnosis initially comes through a series of glucose tests, establishing how the body responds to the glucose (1).  These tests come in two forms:

• Fasting plasma glucose test, where the glucose levels are measured after 12 hours of fasting.
• Oral glucose tolerance test, where the person is given a glucose fluid test and the glucose levels in the blood are measured at regular intervals to see how well the body does in taking control of the glucose.

There are also various blood tests that medical practitioners are advised to carry out (2). 

Type 1 diabetes can develop quickly (3), although I do question whether this is that the final destruction of the remaining 10% of beta cells happens quickly and that the actually build up of the disease from a fully functioning 100% beta cell position happens over a much longer period of time.

Treatments for type 1 diabetes

Insulin replacement therapy

The standard treatment for type 1 diabetes is insulin replacement therapy.  Insulin has been available since 1921 and this is delivered to the body through either subcutaneous injection or insulin pump.  The aim is to monitor blood glucose levels and use insulin when this gets too high so that blood glucose levels are kept within the 2010 American Diabetes Association Clinical Guidelines of 80-140mg/dl (2).

Self-injecting insulin becomes a daily occurence for most type 1 diabetics (image courtesy of Jill A. Brown)

The risk of this treatment is that it can be easy enough to mismatch the insulin with the food, and physical activity going on at the time so that blood glucose is taken too low and hypoglycaemia occurs.  The list of possible signs and symptoms of hypoglycaemia are too numerous to list here and are frequently contradictory (both feeling hot and feeling cold are on the list as well as rage, irritability, depression and crying).

In the early days of insulin replacement therapy the insulin was extracted from cattle or pigs.  However, extraction of insulin was difficult, erratic and expensive in the early 1920s and until the process was improved there were, for a brief 2 years, attempts to extract insulin from fish instead, which was technically easier though apparently logistically more difficult (4).  Fortunately things have moved on significantly and insulin that is used to treat type 1 diabetics is now produced synthetically.

While the majority of type 1 diabetics use injections as the method to deliver insulin into the system, insulin pumps became available in the 1970s.  According to the ever-helpful Wikipedia, the pump provides continuous infusion of insulin and therefore removes the need for multiple injections throughout the day making it appropriate for intensive insulin therapy.  If you are interested in pumps you can learn more from Diabetes.co.uk.

Other possible treatments

There are a couple of other treatments which are, at the moment, still considered to be experimental.  These include pancreas transplant and islet cell transplant.  Most success with these transplant methods has come with islet cell transplant. 

The islet cells are the beta cells in the pancreas which produce the insulin.  These can either be transplanted from another source or can be “built” using the patient’s stem cells – use of the patient’s own stem cells is more successful as the new cells are less likely to be rejected by the body.  These cells are injected into the liver which takes on the role of the pancreas in the release of insulin.  As far as I can see from the things I’ve read, this use of the liver is partly because the liver is more accessible!

Islet cell transplant is still in the experimental stages but a study carried out in 2005 showed that a year after the transplant 80% of the patients were insulin independent (didn’t need to rely on insulin replacement therapy) (5).  Of course, other things have to be done as well to stop the body just attacking and killing these new, transplanted, cells.

Exercise issues for type 1 diabetes sufferers

When a person exercises, their muscles utilise the glycogen stored within the muscles as energy for those muscles.  As these stores become depleted the liver is triggered to release glucose from its big glucose store into the blood stream.  This elevated free glucose in the blood triggers the insulin to be released by the pancreas and ultimately this free glucose is taken to the muscles to continue providing an energy store and to replenish them for your next muscular challenge.

For a type 1 diabetic the challenge is that the insulin isn’t produced to deal with this and they can rapidly become hyperglycaemic as a result of their workouts.  How significant this increase in blood glucose is will depend on how experienced they are at training and the intensity of their training. 

The following gives an idea of what blood glucose response comes from different exercise levels (6):

• Untrained individuals, high and low intensity: marked increase in blood glucose levels.
• Trained individuals, low/moderate intensity: minimal increase in blood glucose levels.
• Trained individuals, high intensity training: marked increase in blood glucose levels which is even higher once reaching anaerobic levels.

Measurement of personal responses is advisable, but Robb Wolf has taken this information and developed some initial recommendations on how type 1 diabetics should moderate their training approach.  It’s an article well-worth reading.

*****

That’s all I’ve got space for this week so I’m going to save up the piece about a possible cure for diabetes for next week. 

The crux of the problem is that diabetes is believed by most to be neither preventable (7) nor curable, yet there is a growing body of anecdotal evidence and a few tangential studies which together imply that it is being successfully cured in people through nutrition changes.  My belief is that if a disease can be cured then it should be possible, with those same interventions, to prevent it occurring in the first place. 

Bibliography

1. Cihakova D: Type 1 Diabetes Mellitus.  John Hopkins Medical Institutions website.
2. American Diabetes Association: Standards of Medical Care in Diabetes – 2010.  Diabetes Care 2010, 33:Supp.1:S11-61 (Executive Summary.  Diabetes Care 2010; 33:Supp.1:S4-10)
3. Cooke D and Plotnick L: Type 1 Diabetes Mellitus in Pediatrics.  Pediatr. Rev. 2008; 29:374-385.
4. Wright J R: From ugly fish to conquer death: J J R Macleod’s fish insulin research, 1922–24.  The Lancet 2002; 359:1238-1242.
5. Bertuzzi F, Marzorati S, Secchi A: Islet Cell Transplantation.  Current Molecular Medicine 2006; 6:369-374.
6. Brooks G, Fahey T, Baldwin K: Exercise Physiology: Human Bioenergetics and its Applications (edition 4).  Macmillan Publishing Company 2004; 193-194
7. World Health Organisation: Diabetes Fact Sheet.  WHO 2011; Fact Sheet 312.

Related posts:

1. Type 2 diabetes
2. Type 1 diabetes: a possible cure
3. Diabetes: an introduction

What is diabetes?

The commonly-known diabetes is in fact short for diabetes mellitus.  A surprise to me was that there are actually other diseases with “diabetes” in their name which don’t have anything to do with the group of diabetes diseases that most people think of when you say “diabetes” – the group which we’re looking at here.

Diabetes mellitus is made up of a group of metabolic diseases which are all characterised by high blood sugar.  For the purpose of this series I am focussing on types 1 and 2, but it is worth being aware that diabetes is not restricted to these.

Frequent insulin injections can become a way of life for type 1 diabetics (image courtesy of Jill A. Brown)

Different types of diabetes

Here is a quick run-down of some of the types (thanks to Wikipedia):

• Type 1 (formerly known as insulin-dependent or juvenile diabetes):  the body fails to produce insulin.  It is recognised as an auto-immune disease.  I’ll explain a lot more about type 1 next week.
• Type 2 (formerly known as non-insulin-dependent or adult-onset diabetes):  whil the pancreas produces insulin, the cells don’t use the insulin properly.  Again, there will be plenty more on this in a couple of weeks.
• Gestational diabetes:  some pregnant women have high blood glucose levels during pregnancy when they haven’t previously had diabetes.  It could be a precursor to type 2 diabetes, but most often resolves after delivery.
• Congenital diabetes:  genetic defects to the insulin secretion.
• Steroid diabetes:  induced by high doses of glucocorticoids – these are not the same steroids as the anabolic steroids used by bodybuilders.
• Monogenic diabetes:  hereditary forms of diabetes caused by mutations in an autosomal dominant gene.
• Cystic fibrosis-related diabetes.

That’s just a taster so, as you can see, almost any disease that is characterised by elevated blood sugar levels is “diabetes mellitus”.

Symptoms of diabetes

The classic symptoms of diabetes are:

• Polyuria – frequent urination (in children this is noticeable if bedwetting recommences),
• Polydipsia – increased thirst,
• Polyphagia – increased hunger,
• Weight loss (most common with undiagnosed type 1 diabetics) (1)

Another symptom which is often how diabetes is spotted in older people is significant changes in eye strength.  Someone I knew was tested and found to have type 2 diabetes after a routine eye examination revealed an unusually profound improvement in short sightedness.  I suppose older individuals may not report other classic symptoms to their doctor, believing that they are simply caused by aging.

If those symptoms are missed then diabetes can lead to more serious conditions or symptoms such as diabetic ketoacidosis (not the same as ketosis) which is often characterised by nausea, vomiting, dehydration and lethargy (1).  If left untreated there is also the risk of things like nonketotic hyperosmolar coma (sometimes known as diabetic coma), cardiovascular disease, chronic renal failure and retinal damage.

How insulin works – why we don’t all have high blood glucose

When we consume carbohydrates these are broken down by the initial digestive processes into free glucose which is absorbed into the blood stream.  When the pancreas senses the elevated levels of glucose in the blood, it responds by releasing the hormone insulin from the pancreas’s beta cells where it is created.

Insulin is a powerful hormone which is best known for its regulation of blood sugar but is, in fact, a general nutrient-storage hormone.  It is involved in the storage processes for other nutrients and the pancreas responds in a similar way to other triggers, such as elevated amino acid levels (2, pp.51-52). 

The insulin indicates to the body where nutrients should be stored, therefore regulating our body’s maintenance and repair at the cellular level.  In the case of elevated blood glucose, the insulin activates blood glucose transport molecules known as GLUT4 which are found in cell membranes and the GLUT4 facilitates the absorption of glucose by the liver (2, pp.63-64).  A recap of glucose storage can be found in my article about different carbohydrate sources.

What happens if a person has diabetes?

I will cover the mechanics of how this insulin-based process breaks down for diabetics in the next couple of weeks, as the different problems with the process define the different forms of diabetes.  However, a question that struck me was why does it matter if we have elevated blood glucose levels?

To answer this I strongly recommend that you read Robb Wolf’s Paleo Solution, pages 63 to 71, for the step-by-step walk through of the complete destruction which occurs but I’ll try to summarise it in simple terms here.

Protein is a fundamental building block for the body, it is what our cells (and therefore our tissues) are made of.  The problem is that protein reacts with free glucose, oxidising the protein and creating a toxic substance known as “advanced glycation end products” (AGEs).  To protect against this our bodies also produce enzymes to undo the AGEs, so usually everything should be fine. 

Usually the insulin would keep our blood glucose levels in check by indicating to, and enabling, the body to store the sugar.  If, for whatever reason, this system breaks down and the body doesn’t put the glucose into storage, the level of free glucose circulating in the blood will rise unchecked.  Unfortunately there is only so much good work the AGE-defeating enzymes can do, so if the system is constantly flooded with free glucose and as a result also floods with AGEs the AGEs will accumulate.  

Why does it matter if our bodies become flooded with (toxic) AGEs?  Well, AGEs can damage proteins (essential building blocks for the body), enzymes (essential to run the body), DNA (telling cells what they do) and hormone receptor sites on the surface of cells.  Since these are the things that ultimately drive the symptoms of aging we get “older” a lot faster and earlier.  Not only that, but AGEs can also kill the beta cells which produce the insulin and the GLUT4 molecules – the essential equipment to stop this happening in the first place – so it ends up making everything much more permanent (2, p70).

So how widespread is diabetes?

A global study of diabetes carried out for the World Health Organisation (3) suggested that in 2000 2.8% of the global population had diabetes and the number of people with diabetes was expected to double by 2030 (partly due to the increase in the population aged over 65 years).  However, when you read the study there is a good chance that these numbers are wrong. 

The percentage was worked out by using data from a limited number of countries and extrapolating to cover the global population.  For example, the data for the Netherlands was extrapolated to cover 13 European countries, including Germany.  There was no data available for developing countries so they assumed that the same relative risks applied and extrapolated existing data to cover the developing countries.  I believe that many developing countries, where diets and lifestyles differ significantly to the Westernised world, may not have diabetes to the same extent and the widely acknowledged risk factors may not be correct.

Despite the implication that this percentage may be overstated, a response to the study and return response by the original authors (4) concluded that this percentage could actually be significantly understated, at least for the Westernised countries.

Either way, this is a significant number of people and a good reason to understand diabetes!

 *****

Bibliography

1. Cooke D and Plotnick L: Type 1 Diabetes Mellitus in Pediatrics.  Pediatr. Rev. 2008; 29:374-385
2. Wolf, R: The Paleo Solution: the original human diet.  Victory Belt Publishing 2010
3. Wild S, Roglic G, Green A, Sicree R, King H: Global prevalence of diabetes – estimates for the year 2000 and projections for 2030.  Diabetes Care 2004; 27:1047-1053
4. Rathman W, Giani G: Response to Global prevalence of diabetes: estimates for the year 200 and projections for 2030.  Diabetes Care 2004; 27:2568-2569

Related posts:

1. Type 1 diabetes
2. Type 2 diabetes
3. Type 1 diabetes: a possible cure

Unfortunately two weeks, instead of one, in the Alps was enough to really mess with my body.

No eggy breakfasts

Food in the Swiss Alps – breakfast

In the Swiss Alps food is not Paleo if you are eating out rather than cooking for yourself, and we were staying on half board for the full fortnight.  Meat is expensive and bread is cheap. 

Breakfast consistently involves:

• Bread – sliced and rolls, most often white but also rye once you cross to German-speaking Switzerland.
• Jam
• Museli with milk

It often also includes yoghurt (my standard breakfast most of the time was museli with yoghurt instead of milk followed by 4 slices of bread with jam) and, in a few rarer places you’ll get the following offered as part of the buffet:

• Cheese (just a couple of slices each)
• Processed sliced meat (usually a little ham and salami, but again, only enough for a few slices each)
• Fruit
• Pastries, such as croissant and pain au chocolat

Food in the Swiss Alps – dinner

Half-board dinners invariably contain four courses in the mountain huts and hostels, reduced to a three course version missing the soup in the hotels, and most often follow this pattern:

• Soup (the less good the quality and availability of drinking water is, the more watery the soup is, providing you with liquid in another format instead – the meat course also becomes more filled with liquid in this situation)
• Green salad (usually just lettuce) with a French dressing (it comes with the dressing already on it, so there is no “leave the dressing off” option – the dressing invariably has gluten in it as well as being very strongly biased towards vinegar)
• Meat casserole or sliced meat (often pork), just a couple of spoonfuls or slices, with pasta (depending on how remote the place is you might get a few vegetables too and on one night we had the treat of potatoes).
• Pudding: most often a scoop or two of ice-cream or a dish of egg custard

As you can probably tell from that, trying to stay Paleo would have resulted in extreme hunger, possibly starvation, and certainly our bodies going into a “famine” mode, given the amount of walking we were doing each day. 

You might get half this amount of meat...

Effects of the diet during the trip

While I am used to eating a higher carb level on my hiking trips, topping off my dinners with extra helpings of chips or crisps in the British pubs, the British breakfast still shines through with its emphasis on sausage, egg, bacon and similar protein-rich foods.  I am not used to having such a carb (and wheat)-rich source of food for all the meals while hiking.

• Bowels:  The effects were almost instantaneous.  Movements became scarce and difficult after day one, despite good hydration, and didn’t improve again until several days later.  I think the problem for that mostly came from the poor levels of soluble fibre in the diet and lack of significant fats.  The occasional poor-hydration day didn’t help.
• Endurance capabilities:  Perhaps the most interesting.  On about day four I found myself hitting the wall partway through the day.  This is something that hasn’t happened to me for some time.  I was fasting from breakfast through to dinner each day but I started seeing spots, feeling like I had a vacuum-packed stomach and a sense of queasiness.  My rational thought became distinctly foggy too.  All common signs of carbohydrate withdrawal.

  When this got really bad, or if we were trying to cross technically challenging ground at the time, I would have a quarter of a protein bar.  These were excessively powerful, yet surprisingly low carb, bars packing in about 400 calories to a bar.  The rest of the time I tried to grin (usually failing, poor Chris) and bear it.  After pushing through for about an hour with this unpleasant sensation I seemed to switch over to the fat burning systems.

This latter problem persisted for most of the rest of the trip, with how bad the effects were depending on how strenuous and taxing the walking was each day.

Post-trip diet recovery

By the end of the holiday I was physically repelled by the sight of bread.  In fact even now, a week and a half later, I still don’t feel tempted by sweet or bready products. 

I decided the best thing to do when I got back, after falling into large bowls of meat with side portions of greens, was to go straight back to a strict Paleo, low carb diet with fasting each day.  This was a problem on two counts:

• I was completely out of energy by early afternoon, struggling to burn fat instead of carbs.
• Hunger had me seeing stars and feeling faint by early evening.

On Thursday, after a horrendous workout, I had a post workout carb intake.  I wanted to show my body that it was allowed carbs but to connect them to specific events.  On Friday morning I felt better than I had all week. 

How I felt through most of the week

Finally, on Friday, I saw sense and had a snack in the early afternoon.  Omelette with a tin of tuna.  It made all the difference in the world.

Now I’m taking it a bit more gently.  Feeding if I need to, timing certain foods to certain events.

Lessons to learn

Here’s a few brief lessons from this:

• Don’t try to go through a full carb withdrawal diet when trying to recover from a physically demanding event.
• Re-teach your body to connect foods to events: excessive hunger = protein and fat; training = carbs.
• Nobody who is converted to fat-burning is immune to converting back in certain circumstances!

Related posts:

1. Lessons learned: low-carb diet for endurance exercise
2. Blog-watch: low carb diets
3. Blog-watch: high protein diets

In my early days of eating Paleo and reading about it, I was struck by a thought about the Venus figurines.  These are carvings from the Upper Palaeolithic period but still early enough to have been part of my studies.  I have to confess though that my real interest and love definitely lay with the much earlier Palaeolithic periods – Lower and Middle – and, more particularly, with how hominids slowly peopled the world.  Once they got into long-term settlements, started showing evidence of modern-style culture with things like trading and stopped being so nomadic I started to lose interest.

Anyway, the thought I had was that Venus figurines very accurately depict obesity and the only way to create a figure that depicts obesity is to know what obesity in humans looks like.  Taking things to their logical conclusion I decided that this suggested that there must have been times of plenty when people were able to get obese.  There’s a whole load of research I’d like to do at some point on this subject (both diet and society-related) and I’d put it on my to-do list for sometime in a couple of years (when some of my existing projects have finished and I hope to have a bit more time). 

Venus of Willendorf (from Wikipedia)

In advance of that, Don at Primal Wisdom had a spurt of blogging about the Venus figurines back in May, questioning whether the type of fatty deposits suggested that people in the Palaeolithic era were already eating grains and whether the figurines really tell us about the diet at the time.  It created a few reactions but I’ve pulled together Don’s articles and one of the reaction posts below to see what other people think.

• Don started out with a long article about the figurines which seems to be questioning whether we really are optimally designed for a high saturated fat, low carbohydrate diet.
• Following on from that first post, a second article by Don showed that one consideration may be that it is just possible to get fat by eating too many calories, no matter whether those calories are from meat, vegetables or more complex processed foods.  On that basis he reckons that it should have been more than possible for women to get obese in times of plenty before grains and processed foods became a regular foodstuff for hominids.
• Finally Don considered a study carried out on rats which suggested that a diet with a higher protein intake (but similar total calories) resulted in greater levels of body fat.  This doesn’t entirely accord with my own experience where I found weight loss (without muscle loss) better when I skewed my reduced calorie intake diet to have a much higher protein percentage so I really don’t know what to think of that, although Don’s reasoning seems pretty sound.
• In response to Don’s posts, Melissa McEwan wrote an article which refers to the growing evidence that hominids were, in some cases, living quite sedentary lifestyles and even consuming some processed grains by the time we reached the Upper Palaeolithic period.  The question being whether this, rather than the protein idea put forward by Don, is a more viable reason for why people knew, intimately, what obesity looked like.

The archaeological records have been moving on a little since I first started thinking about this, but really this goes back to the heart of what I wrote about earlier this year (in parts one and two).  For me, the Paleo diet is a framework and the specific question of whether people in the Upper Palaeolithic period ate grains (as opposed to early hominids in the Lower or Middle Palaeolithic, for example – how early do we stop the evolution clock?) is not as important as the actual considerations of which foods we do or do not handle so well.  That is something which I think has to be considered on an individual basis.

What do you think?

Related posts:

1. Blog-watch: Diet-related links association
2. Blog-watch: low-carbohydrate diets
3. Blog-watch: paleo diet links

This week I’m going to pull together some conclusions about what that might mean for our diet and training.  Hold onto your hats for a rollercoaster article, ladies!

Some brief revision of the hormone cycle and the hormones

I’m not going to go into too much detail repeating previous material so a quick read of my posts about the menstrual cycle hormones and what the hormones do may help.  However, I’m going to kick off with a quick refresher of the main characteristics of the female sex hormones.

Progesterone

• Promotes protein catabolism (you can get more energy from protein than usual)
• Inhibits uptake of glycogen to the muscles
• Research suggests that performance in endurance sports is best when the oestrogen:progesterone ratio is high, though this seems to potentially be irrespective of which of them is elevated.

Oestrogen

• Promotes glucose availability and uptake into the muscles.
• Improves ability to burn fat for fuel.
• Suppresses protein catabolism.
• Oestrogen deficiency can cause impaired regional blood flow when exercising, but I wonder if this is actually oestrogen deficiency in relation to progesterone?

Hormone-based contraceptives

• Results in elevated progesterone hormone for three weeks in every four.
• Potentially high progesterone to oestrogen ratio for those three weeks.
• The fourth week (when no contraceptive pill is taken) the body undergoes hormone withdrawal – I’m unclear exactly what happens but the implication is that both hormone levels drop off – most noticeably progesterone which has been unusually high.

Fitting this into our contraceptive-skewed menstrual cycle

To say that I have been dismayed by the conclusions I reached would be an understatement.  My conclusions suggest that even our contraceptives are perpetuating the myth that women are only good at endurance work.  Although this may also be an explanation for why it is that so many women seem to excel at endurance activities. 

For this analysis I’m working off a typical 3-weeks-on-1-week-off cycle that you would see with the combination pill.  For those with a longer-term hormone intake, you probably want to take my conclusions for weeks 1-3 and extend them to “all the time”.

Weeks 1-3 (while taking the contraceptives)

• Elevated progesterone: oestrogen ratio means that endurance sport performance should be excellent.
• Protein catabolism should be excellent due to the high levels of progesterone.  This could well explain why I can subsist quite happily on a diet with macronutrient ratios of 70:5:25 (P:C:F) when Chris would just fall over trying to base so much of his diet on protein.
• Uptake of glycogen to the muscles is inhibited.  This is bad on two scores:  first, any carbs you take in won’t be processed effectively and are quite likely to end up in fat reserves unless your muscles are crying out for glycogen (eg. you just finished a really heavy resistance session and the muscles are really badly depleted); and second, recovery post-workout may be less good if you’ve done a resistance training session since your body may not be effectively replenishing glycogen stores.

I’m assuming that the oestrogen included in the combination pill ensures that those of us taking it don’t suffer from the poor regional blood flow which is characteristic of oestrogen deficiency.  However this may be something to consider when taking a contraceptive which is solely progesterone-based, such as the progesterone-only contraceptive pill.  Poor regional blood flow could impair recovery during and post workout. 

Of course it could be that the poor regional blood flow comes from particularly elevated progesterone over oestrogen, rather than simple oestrogen deficiency.  If that is the case then it could explain why women perform better on full body workouts.  No single body part is taxed for too long, so that there is a reduced need for instant recovery (from the blood flow) and instead plenty of time for recovery (until the next workout when you use that muscle group again).

Week 4 (withdrawal week)

• Protein catabolism drops off a little so that high protein diet may need tweaking for the week to keep you feel satiated.
• Endurance performance might drop off as progesterone levels decrease, so this may not be the week to run a marathon and aim for a personal best time.
• Glycogen uptake to the muscles will improve, so you’ll probably find yourself more able to handle carbohydrates without it going straight to your waistline.  That is provided you are being active.  Warning though that this is a few more, not carte blanche to stuff yourself with cake, and if you are sitting at your desk all day you’re not really depleting your glycogen stores so this point is null and void.  They need some depletion to have space for the glycogen you then ingest (via the carbs).  This benefit may also make this a better week for resistance training, especially higher rep bodybuilding-style work where you want to exhaust the muscles and then ingest higher carbs to spike insulin and build muscle size.
• If we assume that oestrogen slowly starts to rise during this week off (with the body coping with withdrawal by starting a normal menstrual cycle again) then the body might be better at burning fat for fuel in this week so some extra fat in the diet (to replace some of the protein) might work well.
• The body is going through withdrawal.  As such it is likely to be under stress, especially at the very start of the week when the withdrawal first hits.  This is followed immediately by a bleed which is another stressor.  Overall we’re looking at a spike in stress hormones which could cause a period of muscular weakness and tiredness.  On top of that, Berardi has referred to a paper which highlighted the inverse relationship between cortisol and testosterone, so in the early part of the withdrawal bleed testosterone levels are probably low and really heavy lifting is likely to be tough.

In summary

For weeks 1-3, when taking the contraceptives, it looks like a diet with a high protein percentage should work well.  Keeping carbohydrates really low except for immediately post workout when glycogen stores are depleted and signalling in the body for replenishing those stores is high.  The body is also likely to cope really well with endurance sports and in the weights room total body workouts could well be the best bet.

Hitting week 4, when undergoing hormone withdrawal, the body can probably handle carbohydrates and fat better so consider replacing some of the protein with fat and allow a little more flexibility with carbohydrates as long as there is plenty of activity going on to keep depleting glycogen stores.  Endurance performance may drop off a little and heavy low rep resistance training should probably be avoided in the first few days (or at least taken carefully to avoid injury).  However, resistance performance may improve in the second half of the week and this could be a good week to do some bodybuilder-style hypertrophy work.

***** 

Unfortunately I’ve run out of space this week to look at the last part of this story.  Look out next week for a final part where I see how my conclusions stack up against information which some of my readers gave me a few months ago.  In the meantime, let me know what you think of these conclusions.

Related posts:

1. Menstrual cycle on the contraceptive pill
2. Blog-watch: impact of the contraceptive pill on performance
3. Blog-watch: interaction of diet and exercise with the menstrual cycle – part two

Coming off a diet – some principles

I have some very basic rules which I apply when I first come off a diet.  I’ve set them out below.

• Ease up the calories slowly.
• Focus on dietary fat to increase the calories.
• Increase “daily” carbohydrates but target them to the pre-workout window.
• Remove the weekly carbohydrate re-feed.

How do I ensure I don't just turn this graph around and end up back where I started?

Ease up the calories slowly

During my diets, my body adjusts to the reduced levels of calories.  While it doesn’t adjust to the extent that my fat loss diet becomes maintenance level, my body would get a shock if I suddenly went back to excessive calories without any prior warning.  It would start storing as much as possible in anticipation that I might go back into a “famine”.

To deal with this I increase the calories with care.  At the peak of a fat loss diet I’m on about 850 calories a day and on an average day outside a diet I would probably consume about 1,300 – 1,500 (with a few peak days when I consume far more than that).  For me a gentle increase in calories is just 100-200 extra calories, increasing by this amount every one or two weeks.

Focus on dietary fat to increase the calories

The nature of my body adaptations to diet mean that I can now process both fat and carbohydrate very effectively for energy.  I have therefore found it necessary to restrict my dietary fat intake as well as my carbohydrate intake to get best results when cutting body fat.  Before Christmas my macronutrient ratios were 70% protein, 20% fat, 10% carbs.

Dietary fat is crucial for good health and my long fat loss diet before Christmas was really starting to show in my menstrual cycle, skin elasticity (also potentially die to a Vitamin B deficit) and a few other things in the last few weeks.  I am aware that if I mix round my macronutrient ratios to replace some of the protein with dietary fat these things start to improve, even at the same calorie level (by swapping a few foodstuffs around). 

I find that the easiest way to move back to maintenance is to keep my diet very similar to my fat stripping diet, therefore controlling protein and day-to-day carbs, and add calories by adding in some fat sources to this.  This time I did it by making my breakfast tuna into tuna mayonnaise for a few weeks, instead of plain tuna, and by using the complete egg, fried, instead of just the egg whites, boiled, with my dinner.

Back to eating my yolks

Increase “daily” carbohydrates but target them to the pre-workout window

I’ve put “daily” in inverted commas here because I really mean “as often as you do a workout”. 

During my fat loss diets I strip all except the most basic low net carb (carb content after deducting the total grams of fibre) vegetables from my diet.  Broccoli and cabbage are the staples.  Once a week I then have a weekly re-feed in the form of a large meal where the additional calories are, as much as possible, from carbohydrates.  This kick-starts my metabolism again and refuels the glycogen in my muscles from a week of glycogen starvation and hard gym work.

Once I’m off the diet I no longer want my muscles glycogen depleted and I’m happy for my body to burn the glycogen during workouts.  I’m not trying to force it to use up the body fat which I’m carrying.  To address this, I put some pre-workout carbs back into my diet but only during the hour before going in the gym.  This will mean that workout days have a bigger calorie intake, but I hope that it nets off against the energy output in the gym.

Remove the weekly carbohydrate re-feed.

This shouldn’t really need to be explained after the last few points.

The intake of carbs before my workouts again should mean I am no longer carb-depleted and don’t need to carb load to deal with the problem.  The general increase of daily calorie intake also means that there is no longer any need to boost the metabolism on a weekly basis.

What happens to my body composition?

My fat loss diets are strict and reasonably extreme (although nothing like the last few weeks of competition bodybuilders and figure athletes).  As a result I would expect some immediate consequences from a change back to a maintenance diet.

Just as I tend to notice a sudden drop in my measurements and weight during week one of a diet and attribute this to the reduction in carbohydrates and the associated lack of water retention in the body, I similarly expect to see a step up in weight and measurements in week one after finishing my diet.  Just enough to reflect the fact that my muscles are better-filled with glycogen (making them a bit bigger) and the glycogen causes the muscles to need to retain more water (increasing their size and weight).

For me this typically looks like about a 2kg increase in weight (just under 4%) and an increase in thigh and glute measurements of 0.5-1cm (ca. 1%).

A final thought

Getting successfully onto a maintenance diet after a strict fat loss diet is a fine balancing act.  I find that continuing the habit of measuring and weighing every week is the best way to get it right.

After expecting the jump up in week one, I expect my numbers to plateau.  If I find they are increasing significantly (or consistently going up a little more every week) then I cut total calories back a bit.  If I’ve been on the same calorie intake for two weeks and my measurements are starting to drop again, I’ll move up another step.

There’s no correct answer to a maintenance diet other than care and vigilance until you’re at a calorie intake where you can trust yourself not to overdo things if you aren’t measuring.

Related posts:

1. Blog-watch: Diet-related links association
2. Top ten tips for writing a weight loss diet
3. What diet is best for losing weight?