Proponents of IIFYM (if it fits your macros) often argue that there are no magic foods and that all calories are created equal.
They claim that as long as the caloric deficit is equated, the type of foods you eat will not impact body composition or health outcomes.
They also argue that the health benefits obtained from a diet are purely due to weight loss itself, not the food composition of the diet.
Now granted, the majority of weight loss will boil down to being in a caloric deficit. I don’t think too many people these days are going argue that apart from the odd keto warrior.
Furthermore, most IIFYM proponent tend to focus mostly on consuming nutritionally dense foods anyway because they are more satiating, so everyone is in agreement there.
However, there is accumulating evidence that what you eat and when you eat can indeed have an impact on body composition and other health outcomes independent of caloric intake.
For example, several studies have shown that certain time restricted feeding regimens can improve markers such as insulin sensitivity, blood pressure, and oxidative stress, as well as increase autophagy and promote anti-aging effects, irrespective of caloric restriction or weight loss [1,2].
In addition, certain dietary components including sulphates, animal proteins, simple sugars, refined carbohydrates, and artificial sweeteners have been found to contribute to intestinal dysbiosis [3-5].
Our gut microbiome is made up of trillions of bacteria and other microorganisms that reside in the lower intestine and colon. The microbiota plays a huge role in our health and serves many important purposes such as strengthening gut integrity and shaping the intestinal epithelium, digesting fibre, regulating energy metabolism, protecting against pathogens, regulating immune function, and brain health [6-10].
When there is an overgrowth of pathogenic or harmful bacteria, yeasts and/or parasites, and too few beneficial bacteria, called dysbiosis, it can adversely impact our health and body composition.
Dysbiosis has been linked to obesity, inflammation, insulin resistance, inflammatory bowel disease, IBS, allergies, asthma, cardiovascular disease, and mental health issues [11-16].
Furthermore, studies have shown that overweight individuals can be metabolically healthy, and lean individuals can present with metabolic complications such as insulin resistance [17-20].
Therefore, the premise that the health benefits of a diet are purely due to weight loss is FALSE!
Ok, so not that we have established that what you eat and when you eat can have a direct impact on health outcomes, where does that leave us in terms of food quality and weigh loss?
Well, in a very recent study published just last month a group of researchers compared the effects of two isocaloric diets where one diet was enriched with nutrient dense foods such as poly and monounsaturated fats, fibre, plant protein, and sugar intake was reduced [21].
What they found was that the nutrient enriched diet not only had more favourable cardiometabolic health outcomes, but they also lost on average 2kg more fat over 12 weeks consuming the same amount of calories!
Now, some IIFYM proponents have already come out and started bashing this study by claiming that the nutrient enhanced group on average consumed slightly less calories and their protein intake was higher.
However, this is really splitting hairs. The nutrient enhanced group only consumed about 1% less calories and their protein intake was only about 20g per day more, which would yield measly 25 calories extra being burned due to the increased thermic effect of feeding.
It is funny how IIFYM proponent usually claim that you should focus on the majors instead of majoring in the minors, but then they start splitting hairs when it comes to defending their position.
A more plausible explanation for the extra weight loss, one that was proposed by the researchers of the study, is that certain foods may enhance weight loss due of the upregulation of genes involved in energy expenditure and downregulation of genes involved in energy conservation [21]. Maybe there are magic foods after all!
This further adds to the body of evidence that as coaches we need to start looking beyond just calories and start paying a bit more attention to nutrient quality once again.
About a decade ago, when everyone was so heavily focused on nutrient timing and nutrient quality, but they were largely overlooking energy balance, driving home the point that energy balance is king was important. From that standpoint we should give credit to the IIFYM crowd where it is due.
However, these days the pendulum appears to have swung too far in the opposite direction, and too many people and their coaches are ignoring nutrient timing and nutrient quality because they are too focused on just counting calories.
As with most things, being at either end of the extreme is not ideal…because the truth is usually somewhere in the middle!
References
- Sutton EF, Beyl R, Early KS, et al. Early Time-Restricted Feeding Improves Insulin Sensitivity, Blood Pressure, and Oxidative Stress Even without Weight Loss in Men with Prediabetes. Cell Metabolism. 2018 Jun;27(6):1212-1221.e3. DOI: 10.1016/j.cmet.2018.04.010.
- Jamshed H, Beyl RA, Della Manna DL, Yang ES, Ravussin E, Peterson CM. Early Time-Restricted Feeding Improves 24-Hour Glucose Levels and Affects Markers of the Circadian Clock, Aging, and Autophagy in Humans. Nutrients. 2019;11(6):1234. Published 2019 May 30. doi:10.3390/nu11061234
- Spreadbury I. Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity. Diabetes Metab Syndr Obes. 2012;5:175–189. doi:10.2147/DMSO.S33473
- Hawrelak JA, Myers SP. The causes of intestinal dysbiosis: a review. Altern Med Rev. 2004 Jun;9(2):180-97.
- Palmnäs MS, Cowan TE, Bomhof MR, et al. Low-dose aspartame consumption differentially affects gut microbiota-host metabolic interactions in the diet-induced obese rat. PLoS One. 2014;9(10):e109841. Published 2014 Oct 14. doi:10.1371/journal.pone.0109841
- Natividad JMM, Verdu EF. Modulation of intestinal barrier by intestinal microbiota: Pathological and therapeutic implications. Pharmacol. Res. 2013;69, 42–51 doi:10.1016/j.phrs.2012.10.007
- den Besten G, van Eunen K, Groen AK, Venema K, Reijngoud DJ, Bakker BM. The role of short-chain fatty acids in the interplay between diet, gut microbiota, and host energy metabolism. J. Lipid Res. 2013;54, 2325–2340 doi:10.1194/jlr.R036012
- Bäumler AJ, Sperandio V. Interactions between the microbiota and pathogenic bacteria in the gut. Nature. 2016;535, 85–93 doi:10.1038/nature18849
- Gensollen T, Iyer SS, Kasper DL, Blumberg RS. How colonization by microbiota in early life shapes the immune system. Science. 2016; 352, 539–544 doi:10.1126/science.aad9378
- Cryan JF, Dinan TG. Mind-altering microorganisms: the impact of the gut microbiota on brain and behaviour. Nat Rev Neurosci. 2012 Oct;13(10):701-12. doi: 10.1038/nrn3346. Epub 2012 Sep 12.
- Patterson E, Ryan PM, Cryan JF, Dinan TG, Ross RP, Fitzgerald GF, Stanton C. Gut microbiota, obesity and diabetes. Postgrad Med J. 2016 May;92(1087):286-300. doi: 10.1136/postgradmedj-2015-133285. Epub 2016 Feb 24.
- Halfvarson J, Brislawn CJ, Lamendella R, et al. Dynamics of the human gut microbiome in inflammatory bowel disease. Nat Microbiol. 2017;2:17004. Published 2017 Feb 13. doi:10.1038/nmicrobiol.2017.4
- Distrutti E, Monaldi L, Ricci P, Fiorucci S. Gut microbiota role in irritable bowel syndrome: New therapeutic strategies. World J Gastroenterol. 2016;22(7):2219–2241. doi:10.3748/wjg.v22.i7.2219
- Carding S, Verbeke K, Vipond DT, Corfe BM, Owen LJ. Dysbiosis of the gut microbiota in disease. Microb Ecol Health Dis. 2015;26:26191. Published 2015 Feb 2. doi:10.3402/mehd.v26.26191
- Aron-Wisnewsky J, Clément K. The gut microbiome, diet, and links to cardiometabolic and chronic disorders. Nat Rev Nephrol. 2016 Mar;12(3):169-81. doi: 10.1038/nrneph.2015.191. Epub 2015 Nov 30.
- Kharrazian, D. (2013). Why Isn’t My Brain Working? Carlsbad, CA: Elephant Press, p. 173.
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