Resistant starch: the missing ingredient? Part 1

Just when you think you have everything in your diet dialed in, something new comes along and upsets your carefully constructed nutrition knowledge applecart. This particular compound has been getting nutritionists a little giddy with excitement for a while, and now it is receiving more and more media exposure causing everyday folk scratch their heads at the new wonder boy. It’s hard not to get swept away in general enthusiasm when our popular morning TV show touts Resistant Starch (RS) as a “sneaky fat fighter”.

Remember when things were simple and we were told to just eat more fibre? Well, that is so 1990s. CSIRO in Australia note that while Aussies eat more fibre than many other Western countries we still have the highest incidence of bowel cancer in the world. They call it ‘the Australian paradox’ (what number paradox is it now? I lose track). So looks like adding more fibre in form of All-Bran and bran muffins into our diet has done bugger all to keep those pesky intestinal cells from going bananas and turning into some evil little suckers. All hail resistant starch.

However, as most of you know, I am naturally a fairly skeptical person when it comes to dietary ‘miracles’, especially when the recommendations to increase RS in our diet from the above mentioned morning program look like this:

  • Eat more canned or soaked legumes such as kidney beans, chickpeas and butter beans.
  • Include more intact wholegrains, seeds and cereals, in your diet e.g. oats, barley corn and linseeds.
  • Eat fruit such as bananas before it’s ripe.
  • Eat salads that have been cooked and cooled, such as potato salad, rice salad and pasta salad.
  • Look for breads and cereals with added resistant starch

So what the hell is it? And are you missing out on this miracle food substance?

The official website named Resistantstarch.comAn Information Portal for Health Professionals (don’t you wish that broccoli had an official website?), gives us this definition:

”Resistant starch is the sum of starch and products of starch digestion not absorbed in the small intestine of healthy individuals”

It is also classified as the third type of fibre (together with soluble and insoluble) by several health agencies, including Food Standards Australia and New Zealand, and its MO is to bypass the normal absorption process in the small intestine straight to the colon where it is fermented by colonic bacteria (which also makes it a “prebiotic”).

There are plenty of resistant polysaccharides (starches) that you won’t find in your average shopping trolley and this is reflected in 4 types of RS. Here is a handy table from one of the published reviews (1) on RS (click for better resolution):

Source: Nugent 2005

Source: Nugent 2005

Kind of makes you wonder whether you should start munching on raw potatoes in spite of what Momma always told you and inflict your bean-eating habits on your nearest and dearest for the sake of digestive health. Or should you just trust the clever scientists who conveniently altered the chemical structure of polysaccharides via esterification in order to escape your digestive enzymes? Why are we doing this again?

Oh yes, the claims. I will be relying on the enthusiastic RS article (2) by an Australian dietician Robert Landon written for the official Resistant Starch website to provide the claims to benefits. My facetious comments will follow for your reading pleasure.

Satiety, metabolic health and obesity

I’ll start with this one because clearly this is the stuff that makes big headlines.

“Recent breakthrough research has linked the fermentation of resistant starch with increased levels of gut hormones (PYY and GLP-1) that play a role in satiety and potentially, long-term energy balance.”

“We believe the fermentation of resistant starch may be an effective, natural approach to the treatment of obesity.” says Dr Keenan, the study author.

You can read the study in question here (3) and decide for yourself if feeding 30 rats a carefully engineered concoction of corn oil, methylcellulose or high-amylose corn starch is applicable to human metabolism or behaviour around food. And more importantly, does the release of those “satiety” hormones correspond with actual satiety? Sadly, the previously mentioned (1) 2005 British Nutrition Foundation review by Nugent (peer-reviewed) mentions that the studies which looked at satiety as the end point appeared “to show a weak or no association between RS and satiety over the course of several hours or an entire day.”

Incidentally, I know of a way to increase GLP-1 and PYY levels in humans in a real world which does correspond with satiety: feed them a high protein diet.

This excerpt from the 2013 review on RS (4) made me laugh:

“The physiological effects of resistant starch make it extremely difficult to assess its impact on weight. Resistant starch increases stool bulk, luminal thickness, and bacterial numbers in the colon. These factors add to overall body weight, perhaps masking any differences that do exist due to resistant starch ingestion”

You know you need a new weight loss strategy if your current progress is easily masked by the weight of your poo. Just sayin’.

And I love it when researchers get excited about postprandial glucose and insulin levels. Sounds like this stuff is pretty important, eh?

“… a number of human studies have demonstrated the capacity for Hi-maize® resistant starch to elicit a positive impact on both postprandial glucose levels as well as insulin response.
Most recently, a human trial with maize-based resistant starch incorporated into test beverages showed effective reductions in the relative glycaemic response without any change in palatability”.

Again,  the review by Nugent is a little more cautious:

“There is a lack of consensus regarding the precise effects of RS on insulin and glucose responses: 15 studies have reported an improvement in these measures following the consumption of a RS-rich test-meal, while 10 have showed no, or a physiologically irrelevant effect. It is noteworthy that, to date, there are no reports of RS worsening insulin and glucose responses.”

Phew, it’s nice to know that at least this stuff doesn’t make our blood sugar go through the roof!

Several more recent studies looked at insulin sensitivity in men and women with slightly better results which were obtained by very high intakes of RS: up to 40-50g a day. A paper of note is by K.Maki et al published in the Journal of Nutrition in 2012 (5). The study subjects this time were human overweight and obese men and women broken into 3 groups: control group who received a digestible starch meal and 2 intervention groups, one with 15g of RS a day and the other with 30g of RS. They had to add the products to their usual daily meals for 4 weeks, followed by a 3 week wash out period and then a swap. They underwent a glucose tolerance test at the end of the study.

Insulin sensitivity between 3 groups. Source: Maki et al, 2012

Insulin sensitivity between 3 groups. Source: Maki et al, 2012

The reason why this study caused a bit more of a stir is because it showed better insulin sensitivity in men with a more achievable dose of RS: 15g/day than in men who consumed starches (do you see a little problem here?). Interestingly, there was no effect in women and there was no effect with higher doses. The big problem of this and other similar studies in my opinion is that their control (the column in black) was digestible starch. So in fact,  any difference in insulin sensitivity was relative to the equivalent in starch consumption in people who already have poor glucose tolerance judging by their abdominal girth.

But seriously, can we come up with a plausible explanation why RS starch may improve markers of glucose metabolism? Sure! It reduces the amount of absorbed glucose. This wasn’t too hard, was it? It’s a bit like comparing nicotine levels in full strength vs half strength cigarette smokers. If you smoke low nicotine cigarettes your nicotine levels will be lower. Hooray! We found a measurable improvement! Ahem, you could just stop smoking, of course.

[To all my sweet potato-loving friends, I am not suggesting that you stop eating carbohydrates. Just pointing out that if the only goal is to reduce glycaemic response one might decide to reduce dietary glycaemic input. Or add more protein. Or fat. And by the way, I consume large amounts of this orangy goodness on a daily basis.]

If you demolish your timber dining chair to shreds and sprinkle it onto your Coco-pops, it will also reduce your postprandial glucose levels. Don’t try this at home, kids.

And since we are trying to keep your family physician happy, how about that pesky cholesterol? While early animal studies were quite promising with significant reductions in triglycerides and total cholesterol, these were not replicated in human subjects. 13 human studies showed that RS had no effect on lipid metabolism (1). Sometimes we need a reminder that we are not rats in cages fed laboratory produced chow. Hang on…

So all in all, I wouldn’t be hanging your hat on RS as a shortcut to winning the obesity battle on a global or individual scale as yet. In my next post I will address the evidence behind RS effect on digestive health and, specifically, colorectal cancer. In the meantime, don’t go crazy with that potato starch.


1. Nugent, A. P. (2005), Health properties of resistant starch. Nutrition Bulletin, 30: 27–54. doi: 10.1111/j.1467-3010.2005.00481.x

2. Landon S, Resistant Starch Review published for

3. Keenan et al (2006), Effects of resistant starch, a non-digestible fermentable fiber, on reduction in body fat. Obesity, 14(9): 1523-34

4. Higgins J, Brown I (2013), Resistant starch: a promising dietary agent for the prevention/treatment of inflammatory bowel disease and bowel cancer. Current Opinion in Gastroenterology, 29(2):190-194

5. Maki et al (2012), Resistant starch from high-amylose maize increases insulin sensitivity in overweight and obese men. The Journal of Nutrition, 142(4):717-723

P.S. I will keep the comment section closed at this stage as I will probably address some of the questions and comments in my next post.



The weight loss conundrum

Disclaimer: this post expresses my personal opinions. Fancy that. On my personal blog too. And guess what, this opinion may even be different to yours. You can let me know if you agree or disagree with the views expressed here. You might even go as far as to tell me that I am wrong. I may or may not care about that. Enjoy reading.

Phew. Now that we got that out of the way let’s talk weight loss. Everyone on the internet knows that the best way to get traffic is to tag your pearls of wisdom  “weight loss tips” and “Jessica Biel’s diet secrets”. I have neither. Sorry. But this post was mostly brought on by the frustration that the topic of losing body mass is still a priority not just in conventional women’s magazines but in ancestral health community.

You know the one: “Yes, I’ve given up grains because Robb Wolf told me to, I don’t eat refined carbs after reading Gary Taubes, I stopped sugar after watching that Lustig’s video and I force down a tablespoon of fermented cod liver oil since attending Weston A.Price conference. I feel great but… How do I lose another 10kgs?”

And of course there is no shortage of available experts on the interwebz:
– eat less carbs
– eat more safe starches
– introduce interval training
– stop HIIT to salvage your burned out adrenals
– eat sauerkraut for healthy gut
– calories don’t matter
– calories matter
– start IF
– use FitDay to track your daily intake
et cetera.

It’s all very sad.

In the meantime the average long term success of most weight loss strategies is around 1%. Yeah, sure, most people do it wrong. They choose the wrong diet (Lemon Detox, anyone?), they choose the worst possible exercise (if you are a female with a cup size C and above, for god’s sake stop running). And they just don’t have the willpower that the new dieter has (sarcasm font). Because the new dieter knows that he/she will be different. I will be in that 1% who does it right and stays skinny ever after. The End.

There are numerous reasons why weight loss strategies fail. And there are numerous reasons why they succeed. Temporarily. You can lose weight in literally thousands of different ways: Paleo, low fat, low carb, low calorie, ketogenic, vegetarian, aerobic exercise, HIIT, IF, bariatric surgery, liposuction…

That’s why the to and fro arguments on which approach is better for weight loss is kinda pointless. YES! YOU CAN LOSE WEIGHT EATING MARS BARS AND DRINKING COKE! (feel free to leave this page at this point and celebrate).

We have this love and hate relationship with a number that determines our body mass. Lily Allen famously said: “And everything’s cool as long as I’m getting thinner”. There is another number that we have become very preoccupied with in the last few decades: serum cholesterol. Chasing that number (down) is the name of the game, mostly by pharmacological means. Of course, you could tilt this snow globe upside down and decide that the number per se is not very meaningful and in fact represents some other pathological process in the body. Ideally you would choose an intervention that both addresses the cause of the problem and pushes that number in the direction you want. A nutrient-rich diet free of processed junk and pro-inflammatory toxins accompanied by reasonable physical activity is likely to address the chronic inflammatory state that leads to dyslipidaemia and therefore drop the dreaded cholesterol numbers down and please your conscientious doctor.

But sometimes it doesn’t get you to the magic 5.5 mmols that your doctor wants to see. Just like your 6 month foray into the Paleo diet fails to get you to that elusive number that determines your weight, size and consequently happiness. Time to go on PaleoHacks and shout for help.

I am not having a go at the desire to be slimmer. Sure, I wouldn’t mind losing a few kgs. I also wouldn’t mind losing my freckles or having bigger hands (it sucks trying to find surgical gloves that fit). Neither affects my sense of self worth.

So for what it’s worth, these are my ideas in relation to weight loss (note, doesn’t say FOR weight loss):

I am overweight? Oh thank you, kind sir, I wish I knew this earlier! Let me just switch to a healthy diet and start running.

1. If your primary focus is weight loss you are already behind the eighth ball. If being skinny was a powerful motivator we wouldn’t have 2/3rds of Western world overweight or obese. Wanting to lose weight tends to screw with people’s heads even with the best foundation: they start stressing (excess cortisol=bad), they start reducing/counting/starving/hating their bland food/exercising at 5am and generally stop listening to the bodies.

Things are quite different when you eat to nourish every cell in your body. Shift your focus to wellness and flip the switch.

1a Unless you have congestive heart failure or chronic kidney disease, chuck your scales. Like now. Get up and throw them in the bin.

2. Start with having a nutrient-rich diet and get rid of junk. Use whatever framework takes your fancy: Paleo, primal, perfect health diet, whole30, Mediterranean, vegetarian (gasp! ). Minimize the “healthy” versions of unhealthy food, you don’t want any food holding you emotionally hostage.

Until you have that down pat, forget the words “Do you have these pants in a smaller size?”

3. Find a regular consistent physical activity you enjoy. I know exercise is supposed to be about torture. That’s ok if you enjoy torture, no judgement here. Do something you can see yourself doing regularly in a year. Or five.

3a. Do not ramp up the volume/intensity of the said activity to accelerate weight loss beyond the level you see yourself comfortably doing long term. Did I hear you say “bootcamp”? Pfft.

4. You cannot fix self esteem issues with weight loss. The two have very little to do with each other.

4a. In the same vein, having weight loss as a dangling carrot in the future can derail your enjoyment of today. Don’t put off activities, clothes or happiness until you get thinner. See point 1.

5. It seems that the thoughts of weight loss frequently return when people are still longing for a six pack in spite of measurable improvements in their physical and mental health. This is where we hit a little snag.

Let’s say you start off in the obese category. Up to a certain point weight loss and health gains go together. Then you reach a state where your body is happy, healthy and well-nourished. To lose more subcutaneous fat from this point will not gain any further health benefit. In fact, you may dip down into negative territory. If you are body builder, dancer, gymnast or any athlete dependent on low body mass this is the risk you have to take. If you are a suburban mother of 2, disappointed she doesn’t look like her graduation photo any longer, you may be playing a dangerous game. If you still choose to continue down this path that’s cool. Your choice. It’s way harder to shift the happy-healthy weight so you may have to pull out all stops. Some of those deviate even further from the path to long term health and wellness. Obviously if you are naturally lean and small you have to flip this scenario 180 degrees. Getting massive past the point of diminishing returns may not be optimal for your body either.

When I see an obese patient I do not have an overwhelming desire to help them lose fat. To me their weight is nothing more but an external manifestation of serious internal issues.  I worry about their risk of heart disease, diabetes, Alzheimer’s and autoimmune conditions. I feel the same level of concerns for the skinny-fat: normal BMI with little muscle and obvious visceral adiposity.

Incredibly sexist and quite offensive to naturally thin women. However we don’t think twice when the ads are turned the other way around.

For a health-conscious and somewhat rebellious community we are still remarkably superficial and eager to conform to the current body image stereotype.

I’ll have what she’s having.

This immortal line from “When Harry met Sally” (YouTube it if you are too young to remember this) is the embodiment of our attitude to weight loss. We fall for it, hook, line and sinker, every time. Don’t believe me? Do the following statements apply to you?

I have tried a weight loss spray (congratulations, if you don’t know what I am talking about)
I have bought/considered buying AbCirclePro
I have done a Lemon Detox Diet
I buy protein bars endorsed by my favorite bodybuilder
I have bought Zumba DVDs to get a “Zumba body” at home
I follow the success stories in a fitness magazine and analyse their diet and training
I ask my girlfriend what she did to lose weight and try to copy her plan

I bet most of us go from “you gotta be kidding me” to “what’s wrong with that?”. In actual fact, all these scenarios are based on clever advertising (featuring skinny models) + our natural inclination to believe in patterns. It is very easy to look at a fit and slim individual and say: “Whatever you are doing is obviously working, please tell me your secret so I can look like you”.

The next natural step is for the owner of this fantastic slim and fit body to say: “Whatever I am doing is obviously working, so if you do the same, you will look like me”. To be honest, I was a perfect example of this self-righteous arrogance myself a few years ago. Teaching 10-15 classes a week as a 20-something fitness instructor, I was happy to share my advice to “eat everything in moderation” to my obviously less disciplined participants.

My previous post on insulin received similar comments.

“I understand that carbohydrates stimulate insulin, and insulin promotes fat storage. But I have been eating sweets, cereals, pasta, cakes, etc. all my life, and I am still skinny. According to your logic, I should be fat and unhealthy. What gives?”

I totally hate you for being able to eat whatever you want. But don’t give your metabolism a pat on the back and go crazy with leftover Easter eggs just yet. You might just pay for it later.

There is no doubt that some people seem to be born with an ability (or a gift?) to consume a box of Krispy Kremes with no consequences. Come to think of it, most people could get away with a lot more dietary indiscretions as children or teenagers. For others, the battle might have started in high school, or in their 30s. Many factors are at fault. You can probably blame it on genetics, it is a fashionable thing to do. The problem with that is that genes are passed down with very little change between generations. As recently as 1989, the prevalence of overweight and obesity in men in Australia was 46.7%. In 2000 it shot up to 60%. I am sorry, but genes do not mutate that quickly!

And since now we hopefully agree that our weight is regulated by hormones, has anything changed in our bodies on hormonal level? Yes. Let me introduce you to insulin resistance, the key player in metabolic syndrome. Think of it as a link between overweight and diabetes. If you remember, insulin’s job is to let glucose into the muscle, liver and fat cells. Insulin resistance means just that: cells, especially liver and muscle cells, stop responding to insulin and do not let any more glucose inside. As a result a couple of things happen. Blood glucose levels go up, firstly because of peripheral resistance (muscle cells close their doors to glucose), secondly because liver cells fail to detect the rising blood sugar and do not down regulate their own glucose production. Double whammy means more glucose floating around your system (=hyperglycaemia). Pancreas try fight the flood of glucose by releasing even more insulin (=hyperinsulinaemia). Does this sound like perfect conditions for putting on some extra fat? (I’ll discuss the causes of insulin resistance another time, but you can be sure that carbs will not be an innocent bystander).

So the road from insulin resistance to diabetes looks like this: peripheral muscle + liver insulin resistance -> hyperglycemia -> pancreas releases more and more insulin -> insulin and extra glucose causes fat gain (mostly around your belly) -> belly fat promotes inflammation which further increases liver insulin resistance -> pancreas gets tired of playing catch up with blood sugar -> blood sugar rises even more -> you get diagnosed with type II diabetes -> pancreas is now burned out completely -> you need insulin injections.

The first few steps can happen before you even know it. By the time you realise that your metabolism is out of whack, your body is churning out too much insulin for an innocuous amount of carbohydrates. Suddenly a piece of pizza, which was your weekly staple in your 20’s, becomes a luxury your waistline can no longer afford. Same principle applies if you are a high carb fitness freak, cruising on the Australian government recommended diet. Your muscles and liver are still sensitive to insulin. You look good. You feel great. Is it possible that you are genetically gifted to avoid all complications of obesity and diabetes later in life? I don’t mean to be a killjoy (I love my cheesecake too!) but with insulin resistance rates estimated between 13 and 30% in Oz, I don’t like your chances.

Insulin: superhero or super villain?


OK (mentally rolling up my sleeves). I will try to make this as basic as possible, mainly not to confuse myself. To the biochemistry geeks: don’t pick on me. If you are a visual learner and don’t like reading too many words (good luck tackling “War and Peace”), scroll halfway down the page for the Insulin Action summary diagram.

It can be a revelation to realise that your metabolism (and therefore your weight) is regulated by hormones. Here you are, religiously counting your calories, looking up nutrition charts and calculating your necessary protein portions, and your own body doesn’t care one bit. I am sorry to break it to you but an uneducated old woman in a remote Russian village is doing a better job in controlling her weight than some of us are. I should know, she is my grandmother.

Insulin could be the most important hormone in our body.

How to keep a tight leash on glucose

The first thing you need to understand is that our blood sugar (=blood glucose) is kept in a narrow range. If it gets too low your body will start sweating, hands slightly shaking, heart rate goes up and you might become less pleasant to be around . If you are thinking that this sounds a lot like a first date, you are right. The same forces are at work here: hormones adrenaline and noradrenaline fire up your sympathetic autonomic nervous system, responsible for our ancient “fight or flight response”.

Other players like glucagon, growth hormone and thyroid hormone get involved. Their combined action is to raise your blood glucose back to normal by breaking down glycogen (stored glucose in the liver). Your body switches to preferentially burning fat for energy and ketones, produced from this process, are fed to the brain and to the heart.

Normally this would be the end of your troubles: blood sugar normalises, your body starts happily eating away on all that fat conveniently stored for such purposes. However, things can go wrong if you have injected yourself with a whopping dose of insulin or if your sympathetic nervous system doesn’t work. Blood sugar dips even lower, brain starts to starve without an energy source in the form of glucose or ketones, and you end up in a coma. Not nice.

High blood sugar is toxic

If your blood sugar gets too high, your body doesn’t like it either. To protect your brain and other cells from toxic effects of glucose, your pancreas release insulin. The primary job of insulin is to take glucose out of the blood and dump it into the cells which are prepared to take it. It sort of reminds me of when my boyfriend tries to clean the room. His main concern is only the mess that he can see: clothes get shoved into drawers, papers shuffled into a pile out of the way. (Don’t get me started on not vacuuming around random objects like a shoe box which because they are clearly too heavy for lifting).

Insulin sweeps the blood with the same nonchalant efficiency. It acts on specific receptors on the surface of muscle and fat cells, effectively opening the door and letting glucose into the cell. In a muscle cell, glucose can be used for energy or stored as muscle glycogen for later. In a fat cell, you guessed it, it is used for forming triglycerides, a.k.a fat. Insulin does not care that the “drawers” are full and you would prefer NOT to store any fat. All it cares about is neutralising the sugary sweet wave of glucose. If insulin did not do its job (like if you have type I or advanced type II diabetes), any high carbohydrate meal would leave you nauseated, confused, delirious and end up in a coma. All roads lead to Rome.

So to re-cap (biochemical terms in brackets).
High insulin =>blood sugar pushed into liver, muscle and fat cells (↑ glucose uptake)
=>blood sugar converted into its storage form the liver and muscle (↑ glycogen synthesis)
=>liver makes fatty acids and releases them as triglycerides (↑ fatty acid synthesis in the liver)
=>fat cells get fatter (↑ triglycerides synthesis in adipose tissue)

Insulin action summary

Incidentally, does anybody else think it’s interesting that we have a whole gang of hormones dealing with hypoglycemia (=low blood sugar) and only one dealing with hyperglycemia (=high blood sugar)? Could this mean that sky high glucose was a rare event from the evolutionary point of view and we didn’t need much back up? Hmmmmm…

So it’s actually quite simple. Let’s say you are a healthy 20-something with bulging biceps and metabolism buzzing like an Energizer bunny. You start your day with 7 weat-bix (because a paid athlete said so) with low-fat milk (because your girlfriend follows nutrition advice from Cleo magazine), washed down with a glass of orange juice. Almost 100g of carbohydrates makes your blood glucose go up, insulin rushes into the blood like a knight in shining armour. Blood glucose gets swept into the cells, and blood sugar levels settle back down. Insulin sticks around for a few more hours though. It tries to keep fat locked inside the fat cells and glycogen stored safely away in the liver and muscles. You have your protein shake “to prevent muscle breakdown” at 10.30am, raise your blood glucose again, your insulin is still up. You conscientiously top your blood glucose up every 2-3 hours because it is the healthy thing to do. Your pancreas happily spits out insulin necessary to cover this continuous influx of carbohydrate-rich food.

If you are young, fit and healthy, it doesn’t seem like a big deal.  Multiply this scenario by 365 in a year, add a few spikes of glucose around Christmas parties, birthdays, a huge sugar tsunami for your mate’s wedding, reduce physical activity, add liver inflammation from alcohol, fructose, vegetable oils. Then continue for the next 15, 20, 25 years. (Any of this reminds you of a family member or a friend?)
How long would it take your cells to develop resistance to these massive doses of insulin?
How long before your pancreas runs out of steam to push more insulin out?
How long before your knight-in-shining-armor-insulin becomes your worst enemy?