April 17, 2013

Not so innocent?

This is probably old news to many you, but I only found out/realised/ woke from a coma yesterday to notice that Innocent Smoothies (among other packaged smoothie brands) are pasteurised. Having been foodless all day due to food poisoning (I may never trust a bramley apple sausage again) I finally decided to brave something late in the day. The Innocent Smoothie had come free with my grocery order the night before, and I thought, well, given I’ve lost a lot of fluid, nutrients etc., that this would be a reasonable option, and easy on the tummy!

At first I thought the smoothie was already past its expiry date (hey, when food attacks you, you pay more attention to things like that), but LO! the expiry date on this FRUIT smoothie was MAY 9th, not APRIL 9th. Clearly, I’m naive to the ways of BIG SMOOTHIE*, as when I examined the bottle more closely it states that it is, in fact, pasteurised. More specifically, flash pasteurised, which relies on heating the juice (or as one paper called it, the SUBSTANCE, mmmmm, I love a yummy SUBSTANCE) at ~ 100 degrees celsius, for shorter periods of time than ultra heat pasteurised (UHT) ‘substances’, so somewhere in the region of 15 – 30 seconds.

From a public health and safety POV, flash pasteurisation is a good thing, killing harmful bacteria and also extending the life of the juice. Quite a few companies have been doing it since the middle of the last century, but it in the wake of the raw foods**, preservative free surge of the mid 1990s, some juice makers, like Odwalla (originally of Half Moon Bay, California, now of Coca Cola) went properly naked, if you will, and sold un-pasteurised juices to be as close to ‘raw’ and ‘fresh’ as possible. This nutritionally well intentioned choice turned fatal when a 16 year old died from the apple juice that was a key ingredient in numerous Odwalla products.

Today in the US, all store bought juices must be pasteurised. The only way to get a properly fresh juice or smoothie is to do it yourself or go to a fancy schmancy fresh juice bar. If neither is an option and you go for bottled what are you getting? The short answer is a lot of sugar and likely, fewer nutrients than you would from fresh.

Manufacturers argue that flash vs UHT is better for the consumer in terms of nutrient retention though the overal benefit seems to be in a better and more ‘natural’ tasting juice/smoothie. A 2009 study from Rutgers University showed a much greater loss of raw materials (antioxidant, anthocyanin and total phenolic content) in juices processed to become frozen concentrate compared to flash pasteurisation (Skahill, 2009) but as the substances underwent further processing to become ‘beverages’, the retention between the two methods was insignificant.

Another recent study hypothesised that it’s more likely the method of extraction and ‘finishing process’ that have a greater effect on the final product than pasteurisation in terms of taste and quality, and should be studied further as many manufacturers search in anger a for closer to ‘fresh-squeezed’ option (Baldwin et al., 2011). Still, some feel that the nutritional loss from any pasteurisation method is worth eliminating where possible and current exploration is focussed around alternate processes like microfiltration, which may further retain the integrity of the fruit and its nutritional value (de Oliveira et al., 2012).

So while flash pasteurisation isn’t a completely evil thing, if you’re a vegan or a rawist (or whatever), it’s likely the pasteurisation process won’t meet your standards of purity and ethics. If you’re going for maximum nutrition, you’re probably out of luck with a bottled smoothie, as the thing that seems best retained is the sugar from the fruits. Sure, it’s OK in a pinch, but I’m hard pressed (fnar) to accept that a 250mL bottle of an Innocent whatsit smoothie *really* gives you ‘two of your five a day’ (another concept that’s problematic, but I digress…) what with any pasteurisation process involved. Your best bet is still homemade or the fancy juice bar round the corner. Or hey, go the totally non fuss way and EAT THE FRUIT WHOLE. Crazy, I know…

A former personal trainer of mine once gave me the advice of “don’t drink your calories”, and much as I love a smoothie now and then, from a nutritional standpoint, I could’t agree more.

* OK, I don’t really believe in a BIG SMOOTHIE conspiracy, stop sending me tin foil…

** raw foodists advocate not cooking any food above 40 degrees celsius

References

Baldwin, E. A., Bai, J., Plotto, A., Cameron, R., Luzio, G., Narciso, J., et al. (2012). Effect of extraction method on quality of orange juice: hand-squeezed, commercial-fresh squeezed and processed. Journal of the Science of Food and Agriculture, 92(10), 2029–2042. doi:10.1002/jsfa.5587

Skahill, B. A. (2009). Effects of Thermal Processing on Antioxidant, Phenolic and Anthocyanin Levels in Blackcurrant Juice Rutgers, The State University of New Jersey, 1–67.

de Oliveira, R. C., Docê, R. C., & de Barros, S. T. D. (2012). Clarification of passion fruit juice by microfiltration: Analyses of operating parameters, study of membrane fouling and juice quality. Journal of Food Engineering, 111(2), 432–439. doi:10.1016/j.jfoodeng.2012.01.021

December 31, 2012

A happy and ‘Fast’ 2013!

Firstly, a big thank you to all the readers, followers and especially comment contributors of Shrokit’s Corner. You’ve driven up my blog stats but more than that, you’ve kept an interesting conversation going both here and on twitter, and that’s been really rewarding for me as a fledgling blogger.

Those of you who found your way here via the BBC Horizon site, hungry for more info on 2:5 fasting after watching the programme Eat, Fast, Live Longer may well know that Dr Mosley has come out with a new book: The Fast Diet

What you may not know, is that this little old blog is featured in it (though I’ve not seen the end product, so I don’t know by how much – if anyone has a copy already, do let me know), and that’s no small thanks to the discussions inspired in the comments section.

As far as my own progress, in early January I’ll be getting back into the Bod Pod and having BGL and cholesterol levels checked. Unfortunately, I’ve not gotten around to checking my IGF-1 levels, for a variety of reasons, but hopefully that will be remedied in the new year (I’m still open to offers of free tests ).

In the meantime, I would like to wish you all a very Happy New Year and I look forward to more discussion in 2013!

December 29, 2012

I’m so full, I can barely move… Now, what’s for dinner?

I briefly checked in to Twitter during a self-imposed hiatus (because, let’s face it, I’m an addict and when there’s something really cool on io9 I have to share it with my fellow Twitizens) and noticed a tweet by article82, that echoed the sentiment of a lot of folks this time of year:

I'm again famished. Is there a reason I get hungrier when I eat more food over the course of a few days?
—
Brian Colquhoun (@article82) December 28, 2012

It’s almost endemic to the festive season what with the abundance of large traditional meals, office parties and a general feeling of eat, drink and be merry. Hyperbolic headlines aside, the British Dietetic Association estimates that the average caloric excess at this time of year is an additional 500 cals per day, which depending on how early the “holiday” eating begins (and continues consecutively) can potentially add up to an extra 5lbs to contend with when the new year starts.

But why do we overindulge, or rather, despite sating ourselves through hedonic eating (that is, for pleasure and not just for nutrition) why do we keep topping up?

Short, lazy, oversimplified answer might be: blame your hypothalamus (naughty, naughty hypothalamus, it always wants something…)

The longer, non-definitive, more complicated, multifactorial explanation involves the hypothalamus, some melanocortins, dopamine, leptin, serotonin, ghrelin, reward centres of the brain that relate to addiction, light-dark cycles, alcohol consumption and host of other external, behavioural influences that will vary from person to person, culture to culture. And maybe tryptophan. Simple, no? (/sarcasm)

OK, there are a lot of crazy words and concepts there, so I’ll try to boil it down a bit and focus on the most prominent bits**, we’ll start with the hypothalamus: The pleasure centre, the passion palace, the seat of seduction (ooh er missus) of the brain.

What’s going on under the hood?

squishy bits in your head via wikipedia

The hypothalamus (meaning, cleverly ‘under thalamus’) resides in the diencephalon of the forebrain in us human types. For such a tiny thing (most descriptions say it’s approximately the size of an almond) it has a huge influence and in some instances, immense control over a myriad of physiological functions, among these are impulses relating to hunger, thirst and sexual desire. The regulating of hunger falls under the remit of balancing the body’s energy needs and keeping the brain powered with glucose. Appetite is largely managed by two parts of the hypothalamus, the ventromedial which tells you when you’re full or satisfied and the lateral hypothalamus from where the sensation of hunger originates [1].

The ‘need to feed’, in and of itself is more intricate than that, but appears to be triggered by neurons in the hypothalamus that detect a drop in the hormone leptin, which is released from fat cells called adipocytes. The inverse appears to be true that with high leptin release levels, the desire to eat gets turned off. There are some theories floating around that when humans are well-fed, the sensitivity to leptin levels becomes dulled, which could be one piece of the ‘overeating’ puzzle [2].

But it’s so yummy!

I bake pies. Conveniently, Mr Schrokit eats pies. And he always has the same reaction to them after eating: MOAR (sic). Now, knowing what I put in them, after a couple of slices, I can’t imagine the leptin levels in his bloodstream are lacking, and one would assume that some anorectic peptides (oversimplified translation: the brain’s in house appetite suppressants) would be saying, “no really, mate, we’re good *burp*. Pardon”. But parts of his midbrain, like the ventral tegmental area, are all, “hey, dude, the party doesn’t have to end, there is more pie, after all…”.

This response to pleasurable and tasty food is not unlike that of potentially addictive drugs, triggering brain reward circuitry by being both rewarding (in taste) and reinforcing (it feels good, why NOT have more), by releasing dopamine from the midbrain.

To quote Mr Schrokit in one of his finer moments, “Dopamine monkey wants more dopamine”. Indeed. While similar to drug addiction, the kind of dependence and tolerance overeating creates, develops over extended periods of time, there is some evidence to suggest that it can also be triggered by binge eating events, and from diets rich in high fat foods [3] [4][5].

Hedonic eating cycle: Adapted from AlsiÃ, J., Olszewski, P. K., Levine, A. S., & Schiöth, H. B. (2012). Feed-forward mechanisms: Addiction-like behavioral and molecular adaptations in overeating. Frontiers in Neuroendocrinology,

What? My cooking’s not good enough for you?!

Apologies, I appear to be channeling my dearly departed Gran (who perfected ‘guilt’, so the rest of you are merely pretenders). She was also a feeder! Aside from taking it as a (joking) affront on her cooking, having grown up during the great depression, she couldn’t imagine why anyone would ever waste food. If she cooked it, you were damn well eating it (no, not the brussell sprouts again…). So even though you were stuffed full to your eyeballs, nan (or mum or auntie) gave you that “look”, and thus you had the second, third etc. helping.

Maybe the holidays with your family is really frelling*** stressful and that triggered a cascade of ‘emotional eating’ [6]. Maybe your resolve to not have that umpteenth mince pie was weakened by that last glass of mulled wine, and you threw caution to the wind. Whatever the reason, your environment, peer pressure and the mood you’re in can very much have an impact on your eating behaviour. You could just simply be relaxed, feeling deserving of some gastronomy fuelled indulgence… vowing to tackle the Crimbo Bulge on January 2nd, or was it the 22nd? Or maybe it was July 2nd, anyway, screw it, it’s the holidays, baby!

Clear as mud?

Far from a simple pat explanation, it’s clear that the physiology, pharmacology and pyschology of eating is no easy matter. And no wonder finding cures for weight gain, eating disorders and obesity (or the behaviours that lead to these states) is both confounding and compelling. Again, I’m aware I’ve glossed over a good deal of detail in favour of digestible amounts of info, but like i said, if you’d like seconds…

And just cause it’s the holidays, a picture of a brain I drew:

Brain, by Schrokit, age 39 (at time of drawing)

** this is simply to say, yes, it’s very very intricate and complicated, and there are a lot of details/specific pathways I’m leaving out in my summary, however, if anyone wants more, I’m happy to go deeper and geekier for you. Yes, I’m that giving

*** yeah, I’m finally watching Farscape

References:

[1] Holt, R IG, Hanley, N. A., (2007) Endocrinology and Diabetes 5th Edition, Blackwell Publishing, pp 254 – 255

[2] Bear, M.F, Connors,B.W., M.A., Paradiso; (2007) Neuroscience: Exploring the Brain, 3rd Edition, chapter 16 pp 510 – 515

[3] Berridge, K. C., Ho, C.-Y., Richard, J. M., & DiFeliceantonio, A. G. (2010). The tempted brain eats: Pleasure and desire circuits in obesity and eating disorders. Brain Research, 1350(C), 43–64. doi:10.1016/j.brainres.2010.04.003

[4] AlsiÃ, J., Olszewski, P. K., Levine, A. S., & Schiöth, H. B. (2012). Feed-forward mechanisms: Addiction-like behavioral and molecular adaptations in overeating. Frontiers in Neuroendocrinology, 33(2), 127–139. doi:10.1016/j.yfrne.2012.01.002

[5] Wise, R. A. (2012). Dual Roles of Dopamine in Food and Drug Seeking The Drive-Reward Paradox. Biological Psychiatry, 1–8. doi:10.1016/j.biopsych.2012.09.001

[6] Doğan, T., Tekin, E. G., & Katrancıoğlu, A. (2011). Feeding your feelings: A self-report measure of emotional eating. Procedia – Social and Behavioral Sciences, 15, 2074–2077. doi:10.1016/j.sbspro.2011.04.056

December 16, 2012

F words

No, not that F word (though I forgive those who know me for assuming that…).

It’s been quite a hectic couple of months, hence the radio silence on the blog. Final year of a pharmacology & physiology degree takes a lot out of you , who’d have thought?

Anyway, the F words that I am thinking about are: Food, Fasting, and Fat. Aside from the interesting things I’m discovering on a physiological level, I have noticed that discussions of weight and different kinds of “dieting” (though you all know I don’t think this is a diet, per se) really bring out some high emotions and sometimes even defensiveness over deeply held beliefs (regardless of evidence).

I’ve also been ruminating on commenter Pete’s point about compliments with regard to weight loss. The way some people have reacted to me, you’d have thought I was previously a wildebeest stapled to two John Candys. Generally, we’re not commenting on the person’s improved health when we compliment weight loss, socially speaking, but on a perceived improved aesthetic. The attitudes towards fat and fat(ter) people, are pretty horrid on the whole which strikes me that we could use some more body positive attitudes towards weight loss and health, rather than just assume everyone wants to be skinny.

People’s motives and politics aside, I try to take a compliment graciously and assume innocence and kindness on the giver’s part.

What’s been less pleasant are the negative reactions. Everything from, “That’s really a stupid and dangerous way to eat” or “You realise you sound like you have an eating disorder” to “How do you know this won’t make your cancer worse?”. The first two comments are moronic at best, though they belie something deeper and far different from caring about wellbeing. The last one, misguided perhaps though to some degree valid, because we’re still in the dark about many aspects as to what causes and indeed exacerbates cancers. As far as my own cancer goes, I try to stay healthy, stay on top of new tumours (not literally, that would be weird…) and limit my stress.

Anyway, because of this, and some of the more negative attacks I’ve had from diet evangelists (blood-type, paleo-slim, atkins etc.), for the most part I no longer use the F word “Fasting“. When people enquire as to the change in my appearance, I explain (major tip of the hat to commenter Gordon) the strategy I’m employing to reduce my overall caloric intake on a weekly basis. As I mentioned in earlier posts, at the beginning of undertaking the 5:2 (or 2:5 depending which days you count first) I was counting everything I ate. Not to be obsessive, but for the data (mmmm, yummy data), and also to get a feel for what certain foods “cost” in terms of calories.

What a lesson in caloric content! It really does matter more than quick tricks, food group exclusion or endless supplements. Calories in calories out has an incredible amount of biochemistry and physiology behind it. Our body weight is regulated so tightly in terms of homeostasis, that even as little as 100 kcal per day excess intake (or lack of expenditure) can lead to obesity over time[1]. Knowing what’s in my food calorically really does help me make better choices, as does eating in a way that can be sustained over a long time.

Remember the Twinkie diet professor? I’m not advocating a diet of twinkies and I realise he’s a sample size of n=1, but it’s some pretty interesting stuff with regard to what being under a certain threshold of calories despite the nutritional content of the food, does to one health-wise.

Both Mr Schokit and I have stuck to this since 11 August (we faltered once for a family wedding, but planned around it best we could), and aside from weight loss (around 1st for him and just over 2st for me) we’ve noticed a few added bonuses, that whilst being anecdotal are pretty interesting:

Over all we both seem to sleep better (though we sleep less on fast days – anyone else have that?)
In the first three months, my skin was miraculously clear (winter has since sent that down the crapper)
We both, for the most part, now eat less on our non-fast days (don’t get me wrong there is the occasional curry/pig out/why yes a second bottle of champagne WOULD be lovely)
The difference between hungry v thirsty; hungry v tired; hungry v bored and hungry v horny (yeah, I went there) is VERY apparent as an intermittent faster
Despite already being proficient DIY cooks, we now pretty much make everything from scratch and love it
We think we’ll pig out after a fast, exact opposite happens… (I’m actually really curious as to what happens to the hypothalamus with extended fasting)
I can live with fewer calories, I can’t live without coffee (that last one has nothing to do with anything, I just thought I would throw it in there)

Non-anecdotally, my cholesterol is down as is my blood sugar (despite all those nasty carbs, go figure…) and I’ll be popping back into the Bod Pod in January to see what my lean/fat ratio is (and have another funny picture taken of me in a swim-cap).

Food wise, we got lazy about experimenting with dishes, as you do, but we have a stock of quick easy recipes to throw together. The greatest life saver? Cup-of-Soup! If you’re a Waitrose shopper, they have a nice range of yummy ones.

Being bread bakers has also served us well, we’ve been able to tweak our usual recipe to get the calorie count down, but still getting fibre (never, ever forget the fibre).

This was my fasting day breakfast, basically a faux Eggs Benedict weighing in at 200 calories:

Food looks more appetising when photographed on a wood surface (may or may not be a fact)

I see this as something I can keep up with, which is what a ‘diet’ is for in the long run. If it’s a quick fix, I’m sure most things will do, but having a strategy of managing my caloric intake and still enjoying my food – yes please.

As some of you may know, Dr Mosley is coming out with a book in January called (I believe) The Fast Diet, which I understand will reference a good portion of the current research around fasting. I have been meaning to do more on the science writing side for this blog, but alas, Uni work has had to take precedence (and I’m not just saying because several of my lecturers are reading…). We’re still also planning to get the Fasting Experiment into our science festival in March. I’ve had quite a few emails asking if I’ll be able to include members of the public in the experiment. It’s unlikely, but if I hear of any other similar experiments going on, I’ll be sure to post here.

Reference [1] Holt, R IG, Hanley, N. A., (2007) Endocrinology and Diabetes 5th Edition, Blackwell Publishing, pp 252 – 253

September 25, 2012

It’s not a diet*

(*The title of this post should be read a la Arnold Schwarzenegger in Kindergarten Cop “It’s not a tumour”)

So 7 weeks into 5:2 (or 2:5 as I like to call it since I think of my weeks starting with fasting and then five days of EATING) and still going strong. I’m a little over a stone down, with Mr Schrokit not too far behind (he keeps calling his jeans ‘fat man trousers’ since he needs to do up his belt a few extra notches inwards…).

Because the overall difference in my appearanceand “result” is so easy to see (though people keep asking me if I changed my hair, got new glasses etc., they can’t seem to pin down the weight loss, but I’m getting compliments galore), when I talk to people about fasting, they seem VERY keen to give it a go. In fact, many of Mr Schrokit’s colleagues are on this so called ‘diet’ and finding it very eye opening about their own eating habits.

But it’s not a diet. The best description I’ve heard so far is from blog commenter Gordon. It’s a strategy, to quote him and I can’t think of a better word for it.

The thing that bothers me personally about so many “diets” is that there is always a culprit who is not the food consumer themselves. It’s one’s genes (which is true in some cases, but far less often than you’d think) or the food industry (don’t get me wrong, I think there are HUGE problems with packaged and prepared food, but lets put politics aside and just look at behaviours) or that we don’t eat like our “ancestors” anymore (again, there are a lot of things wrong with the current fashion of saying we should eat like hunter gatherers, or only eat fat & protein, but I’ll tackle those in another post) or that sugar is the root of all evil.

None of these however, address the simple observation, that in modern culture, most of us simply eat too much, full stop. Aside from eating a healthy balanced diet, whatever all the trendy diet books tell you, weight control is really about the aggregate amount of calories you consume in the long run (my next post will address this very specifically, so hold fire on comments if you can…).

I’ve mentioned this before, but the thing that fasting does seem to do (other up for debate medical benefits aside, for the moment) is help one get back in touch with actual appetite. For example hungry versus bored, or hungry v tired, hungry v craving and most of all, hungry versus thirsty all seem a bit more obvious after fasting a couple of days.

Now everything I have posted so far, is quite obviously my own anecdotal experience and should not be taken as anything more than that. Fortunately, my own progress and research into how this works, has inspired many in my university to take a closer more scientific look at fasting, so I have lots of posts in the oven, and I’m looking forward to more conversations with you all!

September 9, 2012

Sunday Power Porridge

I thought it might be time to share another recipe, since anyone who is following & trying my recipes (brave souls) might be bored of kale and PRAWNS (sorry, Dr B, I’ll never say ‘shrimp’ again ).

Today, both Mr Schrokit and I were peckish earlier in the day than we usually are. We’re still doing consecutive days and yeah, still finding the second day more challenging/crankiness inducing. I perused some recipes to find something breakfasty that still allows us calories for the evening, so I settled on an adapted porridge recipe from the app Cook This Not That. Again, I’m not entirely convinced that their recipes, followed to the letter, are as low cal as they say (for one, they always seem to give recipes which yield 4+ servings, so you’d have to really watch how you divide your portions and also if it’s just one or two of you, do you really want the leftover temptation?!), but they are a good baseline from which to start, and they are pretty creative dishes.

Flavour goes a long way towards making dishes more satisfying, and porridge itself can be very filling without tons of extras. We started with cooking plain rolled oats about 1/2 cup (or 40.5g) per serving, in water (2:1 water to porridge if you don’t want it too runny), 1/2 tbsp (or approx. 8g) peanut butter (the kind with no extra crap added, just, um, peanuts), 1/2 tsp (or approx. 4.something g) of honey, with ground ginger, cinnamon and clove to taste (sprinkled, no accurate calore count, so I’m just saying negligible for our purposes as we’re talking *very* minimal).

The whole dish came in at approximately 212 calories per serving, definitely leaving wiggle room for dinner later (likely kale centric, boy does Mr S like his kale…). If you wanted to jooj it up a bit more and feel you want to make it more bulky as your only meal (on Horizon, Dr Mosley had mentioned doing breakfast as his one meal on days he worked/fasted), some of the suggestions are: almonds, bananas, coconut milk or berries.

Sadly, no picture today as we were clearly too hungry to snap any before tucking in, so here are some generic rolled oats:

Oats (sorry, couldn’t be more original)

You might have noticed the hyperlinks with my porridge ingredients, in addition to tracking in Livestrong, I double check with the site Nutrition Data. The cool thing about ND, is the breakdown of foods in terms of nutrition, in addition to having quite specific search criteria. So for instance, if you were looking for a food that was high in fibre and say, vitamin C yet low in sugar, you set those parameters and voilá: You get the humble Avocado. It’s a pretty helpful tool if you’re going for maximum nutrition during your fasting/calorie restricted days.

Another great tool is Wolfram Alpha

Nothing whatsoever to do with food, but helpful for translating American to everyone else in terms of measurements in recipes.

September 3, 2012

What the IGF?

No, it’s not a new swear word, but since the Horizon programme and the start of my own 2:5 experiment, many people have been asking questions about what exactly IGF-1 is.

This is probably most relevant for those taking up 2:5 way of eating (I’m really not keen on calling it a diet**) for reasons other than weight loss.

IGF-1 levels are implicated in quite a few diseases, and while no claim is being made that reducing IGF-1 levels is a magic bullet for modern ailments, there is a growing body of evidence that it can impact some cancers, cardiovascular function and the reversal of neurodegeneration and perhaps even slow down the ageing process itself.

The basic definition of IGF-1, or Insulin-like Growth Factor is that it’s a protein, more specifically, a hormone or chemical messenger (and yes, that’s a wikipedia link for those of you who like that sort of thing…). As the name suggests, it’s ‘like’ insulin from a molecular structure point of view. The two can share similar signalling pathways, but diverge in so far as biological function (Dupont et al 2001)¹.

In plain English, they may look alike, respond to similar stimuli, but act very differently.

IGF-1 also phosphorylates (fancy science word for switching protein enzymes on and off, potentially changing their shape and function) group of substrates called IRS (insulin responsive substrates). They can possibly allow for more (or fewer) interactions as they increase (or decrease) the number binding sites and overall responsiveness (Wilcox, 2005)². Clear as mud, right?

In terms of specific diseases, there have been some interesting findings in recent years concerning IGF-1 and its impact on ER (oestrogen) positive breast cancers, enough to warrant clinical trials. According to Newman et al. (1992) ³, IGF-1 is required in order for oestrogen influenced developmental activity in mammary ducts (i.e. ductal breast tissue growth), in addition to impacting actions of progesterone. A summary article goes on to discuss the direct impact of the IGF-1 pathway on breast cancer (J. Smith et al, 2011) ⁴. Multiple trials, including in vivo animal studies, in vitro experiments and testing women with BRCA gene mutations, show correlations of high risk for breast cancer alongside increased IGF-1 activity.

This could mean huge things for treatment going forward. It would appear that regulating IGF-1 may have fewer hormonal side effects than some current breast cancer interventions, like Tamoxifen (which among other things can cause early or pseudo menopause in premenopausal women with BC) which suppresses oestrogen .

My first BC diagnosis was Stage 2 ER/PR+ invasive ductal carcinoma, since my time machine is broken, I can’t go back to 2008 and see what my IGF-1 levels were (and it doesn’t appear they were tested in the blood work prior to surgery). But I am getting current levels checked, in addition to having my latest barrage of scans to hand, so I’ll be very curious to see what impact 2:5 fasting/eating has on the related data.

Finally, apologies for lack of recipes and food pictures this week. We’ve not gone outside our new comfort zone of kale and quesadillas, yet

**************

¹DUPONT, J., KHAN, J., QU, B.-H., METZLER, P., HELMAN, L., & LEROITH, A. D. (2001). Insulin and IGF-1 Induce Different Patterns of Gene Expression in Mouse Fibroblast NIH-3T3 Cells: Identification by cDNA Microarray Analysis. Endocrinology, 142, 1–7.

²Wilcox, G. (2005). Review Article: Insulin and Insulin Resistance. Clin Biochem Rev, 26, 19–39.

³ Ruan W, Newman CB, Kleinberg DL. Intact and amino-terminally shortened forms of insulin-like growth factor I induce mammary gland differentiation and development. Proc Natl Acad Sci USA 1992; 89: 10872–10876.

⁴Smith, J., Axelrod, D., Singh, B., & Kleinberg, D. (2011). Prevention of breast cancer: the case for studying inhibition of IGF-1 actions. Annals of Oncology, 22(Supplement 1), i50–i52. doi:10.1093/annonc/mdq666

** Speaking of diets, I feel it’s time to revisit my disclaimer: I’m a neurophysiology & pharmacology student, researching Parkinson’s. I’m not giving medical advice, or trying to tell people how to fast/diet/whatever. Inspired by the Horizon Programme, I decided to ‘self-experiment’ if you will. This has now blossomed into a project that will be run at my University what with that fancy scientific method, and all… I’m interested in data, neurodegenerative disorders and what steps I can take in my own lifestyle that will decrease my occurrences of breast cancer.

I’m not interested in pissing contests about “diets”, however, I will correct misinformation (and there’s a lot of it in the comments, it’s inspiring loads of new blog posts…). I’m thrilled that people are coming here for a discussion about fasting and the Horizon programme, and I love a good healthy debate, however, I will starting shutting commenters down for promoting pseudo-science based diets, atkins evangelising or those other otherwise trying to play dietician (unless you are one) by telling people how and what to eat. I personally am not advocating any dietary pattern and I’d encourage anyone with medical issues to consult a doctor before embarking on any major lifestyle or nutritional change, especially where reducing calories is involved!

Schrokit's Corner