Defining Food Allergy vs. Food Intolerance - IIFYM - IIFYM

Defining Food Allergy vs. Food Intolerance


 

There is growing interest in the area of food allergy and food intolerance: in the United States, 25% of adults believe they have a food allergy, despite the actual incidence rate of diagnoses being 2-3% (1). A common issue which explains such a discrepancy between diagnosis rates and self-reported incidence is the interchangeable use of terms like “food allergy” and “food intolerance”. So, let’s get the terminology straight so you know where you stand.

(Side note: Drilling down your diet needs is crucial, it all starts with macros. Click here for you free macro split with our macro calculator.)

An adverse reaction to food is defined as toxic or non-toxic; non-toxic reactions are differentiated into reactions mediated by the immune system [food allergies], and reactions not involving the immune system [food intolerances] (2).

Allergies can be further divided into those mediated by the antibody IgE – which stands for ‘Immunoglobulin E’, and is a type of antibody released by your immune system in response to an allergen – and those mediated by other immune responses.

Taken together, we can break down the definitions as follows:

Food Allergy: a specific immune system response to a given food which is reproducible each time the food is consumed, is not dose-dependent [i.e. occurs with trace exposure], and onset is typically within 0-2hrs of consumption of the culprit food (1). For example, an anaphylactic response to peanut consumption, or atrophy of the villi [brush-like borders on the surface of the intestines] in Coeliac Disease in response to gluten ingestion.

Food Intolerance: a reaction to a food independent of an immune response, typically as a result of either an enzymatic deficiency or a pharmacological reaction (2). A food intolerance may not be reproducible and is often dose-dependent (1). Examples include lactose intolerance from a deficiency in the enzyme needed to break down milk sugars, or a pharmacological response to caffeine [i.e. you run to the bathroom, or get the jitters].

Most adults with an IgE food allergy are aware of the fact and have been diagnosed – this is because IgE-mediated food allergies typically develop in early childhood (2). The most common IgE food allergies include eggs, milk, peanuts, tree nuts, wheat, fish, and shellfish (1).

However, allergic reactions to milk, eggs, and wheat typical in children are often “outgrown” by adulthood, meaning tolerance to the food is acquired (2).

If you’re not sure, there are two questions which can quickly determine whether you need further testing for food allergy:

  1. Does a reaction happen every single time you eat a particular food?
  2. Is the reaction immediate?

Our coaches often hear complaints from clients about suspected food intolerance, but if the answer to the above questions are positive, then our coaches recommend you see your doctor with a view to having some diagnostic tests performed.

This point cannot be overemphasized: recent evidence shows that there has been a significant increase in people self-reporting food allergies in the U.S. without obtaining a medical diagnosis (3).

Given that there has been no increase in actual physician-diagnosed food allergy (3), we can infer that in reality what people are self-reporting as “allergy” is more likely a potential food intolerance. So, what is the likelihood of you having an intolerance to a given food?

Beware of “Food Intolerance Tests”

 

food intolerance

 

The use of blood tests which measure the response of a particular antibody – immunoglobulin G [IgG] – to determine food intolerance has increased in popularity. IgG, like its counterpart IgE, is an antibody released by your immune system and is the most abundant antibody in the body, found in high concentrations in blood. However, there is little evidence to support the use of IgG tests for diagnosing a food intolerance (4, 5).

One of the issues with studies using IgG food testing to determine food intolerance is that the studies often look at the subject with Irritable Bowel Syndrome [IBS], and commonly result in the elimination of foods like cow’s milk dairy and wheat, which are associated with symptoms of IBS. That there is then an improvement in symptoms does not of itself retrospectively validate IgG testing.

In addition, large population research shows wide variance between the exposure to a food and actual symptoms correlating with elevated IgG (6). IgG levels are also elevated in otherwise symptom-free, healthy individuals, indicating that the elevation in IgG may be a reflection of recent exposure to a food, and in fact, represents immunological tolerance (5).

The bottom line is that there is little evidence to support clinical efficacy to using IgG testing to ascertain a food intolerance. Save your money. If you suspect you have a food intolerance – for example bloating after certain foods – often what needs to improve is diet quality. Our coaches at IIFYM.com can help you modify your diet to address the issue.

Do You Really Have “Wheat Belly”?

By “wheat belly”, I mean sensitivity to wheat gluten – a common complaint in self-reported food intolerance – not Coeliac Disease [CD]. CD is an autoimmune condition where ingestion of the protein gluten common in wheat, rye, and barley, causes an immune reaction which leads to atrophy of the villi [a brush-like border on the intestinal surface required to absorb nutrients] (7).

It is a debilitating condition with symptoms including diarrhoea, weight loss, abdominal pain, anaemia, and bone demineralization (7.). It is also diagnosable through testing, so if you have any of those symptoms you should consult your doctor.

Aside from CD, however, there is research showing symptoms – including abdominal pain, bloating, and diarrhea – in subjects in response to gluten ingestion, but without any of the diagnostic criteria for CD (8).

For many people, the issue may not be a food intolerance to gluten as much as the sheer quantity of refined flour in the diet.

This led to the term “Non-Coeliac Wheat Sensitivity” [NCWS], but it’s existence was debated and it was believed to be a manifestation of IBS. Recently, however, NCWS has been confirmed as an independent condition defined by specific, measurable immune system responses (9).

Subjects self-reporting wheat intolerance, but without CD, showed elevated markers of immune system activation and intestinal cell damage which differ to those found in CD (9). These symptoms improved and the immune markers normalized on a gluten-free diet (9). So, it does appear that a specific NCWS phenotype does exist, however, it is diagnosable by reference to these markers.

It is also highly likely that perceived food intolerance to gluten is, in fact, symptoms of impaired FODMAP breakdown [FODMAPs are a group of short-chain carbohydrates which can be difficult for the digestive system to break down]. In a trial of IBS subjects, reintroducing gluten to their diet had no effect on symptoms when FODMAPs were restricted (10).

Food Intolerance to Wheat or Overall Dietary Consumption?

 

food intolerance

 

For many people, the issue may not be a food intolerance to gluten as much as the sheer quantity of refined flour in the diet. In one trial, consumption of 16g/d gluten caused intestinal symptoms in non-Coeliacs (11) – that’s 2 slices of bread and a muffin per day.

In both these trials, the sensitivity to gluten was not reproducible and symptoms were not specific to gluten (10, 11). This strongly suggests that gluten is not likely to be the cause of symptoms in the manner in which the lay public are being led to believe by fad diets.

Addressing diet quality is the lowest hanging fruit, fewer muffins, more vegetables, legumes, fruit and other nutrient-dense carb sources over refined flour products, and you might find symptoms disappear quickly.

Our coaches at IIFYM.com work with their clients not just to improve body composition, but to improve their health through better diet quality. If food intolerance symptoms persist, then given the overlap between IBS, gluten, and FODMAPs, it could be that FODMAPs are more an issue than gluten.

FODMAPs

The acronym FODMAP stands for Fermentable Oligosaccharides, Disaccharides, Monosaccharides, and Polyols (12). It encompasses a group of compounds, not any single dietary entity (13). Humans lack the enzymes needed to break down oligosaccharides, and they pass to the colon where they are fermented by bacteria. The gas generated from fermentation is implicated in causing symptoms of bloating, pain and flatus (12).

IIFYM blueprint

The main disaccharide is the milk sugar lactose, and there are ethnic variations in tolerance to lactose due to a higher prevalence of reduced lactase enzyme activity in certain populations, for example, Asians (12). Monosaccharides and polyols are simple sugars, and they have an osmotic effect in the small intestine, pulling water into the small bowel and causing distention and associated symptoms of IBS (12).

IBS is characterized by abdominal pain, distension, and alterations in bowel habits on a spectrum from diarrhea to constipation, including a mix of both and periods with normal stools, but these symptoms occur in the absence of biochemical, structural or metabolic abnormalities (14). Fermentation of FODMAPS has been implicated in generating food intolerance symptoms of bloating, pain, and distension (15).

It is important to note that as a Functional Gastrointestinal Disorder, IBS is defined as a disorder of gut-brain interaction; psychosocial factors influence GI dysfunction in IBS and patients with IBS frequently present with accompanying psychological disorders, in particular, anxiety and depression (16; 17).

This is important because many of the underlying potential mechanisms of food intolerance observed in IBS also occur in healthy people.

FODMAP and IBS

 

food intolerance

 

For example, FODMAPS exert an osmotic effect in all individuals, however, subjects with IBS appear more susceptible to colonic distention from gas generated from fermentation, and from osmotic effects causing increased small bowel distension, than healthy controls (18).

Increased gas production on a high FODMAP diet occurs in both healthy subjects and subjects with IBS, however, only in IBS subjects does prolonged hydrogen production result in increases in abdominal pain and/or bloating (19).

Subjects with IBS and healthy subjects both produce the same amount of gas, but the increase in symptoms of food intolerance is only observed in persons with IBS (20).

One of the underlying issues in IBS may be reduced levels of bacterial species in the gut specializing in the degradation of FODMAPS, which may contribute to visceral hypersensitivity and abdominal pain symptoms (21; 22).

…lactose is also a FODMAP, and thus symptoms associated with lactose ingestion may indicate IBS.

While diet quality is not specifically implicated in IBS symptoms, we know from research into gut bacteria that the typical Western diet pattern – high in refined carbs, low in fibre, high in animal fat and protein – leads to reduced levels of these beneficial bacterial species (23).

Addressing diet quality is, again, an important first step, and the initial approach to suspected IBS/FODMAP food intolerance is [after excluding other potential food intolerance] to make preliminary dietary changes in relation to fatty and spicy food, alcohol and caffeine intake, and general healthy eating and lifestyle patterns (24). If you remain symptomatic, then the advice would be to consult a Registered Dietitian to be guided through the clinical low-FODMAP diet.

Is the Devil Really in the Milk?

There is no doubt that cow’s milk allergy is one of the most common food allergies in children, but as noted earlier it is typically outgrown and adults develop a tolerance (25). It’s important to distinguish lactose intolerance – a diagnosable condition – from self-reported lactose or milk intolerance, as many people with self-reported food intolerance show no signs of lactose malabsorption (26).

This has led to the suggestion that people self-reporting cow’s milk food intolerance may be reacting to the protein, not the lactose. The theory relates to different types of protein in cow’s milk: “A1” casein found in Europeans or Holstein cows commonly used in industrial milk production, and “A2” casein found in African, Asian, Jersey or Guernsey cows (27).

Studies have suggested that a protein produced from digesting A1 casein may cause gastrointestinal symptoms: a trial in China found increased symptoms in subjects consuming mixed A1/A2 milk compared to A2 milk alone (28).

However, these symptoms were most significant in subjects with lactose intolerance and thus make it difficult to differentiate. Another trial comparing exclusively A1 vs. A2 milk consumption found no significant difference in subjects except in those with self-reported lactose intolerance (29).

Overall, it is difficult to give credence to the A1 vs. A2 debate due to limitations in the studies and the greater likelihood of susceptibility in subjects with lactose intolerance. Processing milk via pasteurization has also been suggested as a reason for dairy food intolerance.

Commercial vs. Raw Milk

 

food intolerance

 

A survey of raw milk consumers revealed that, despite only 5% having a diagnosis of lactose intolerance, many believed it was easier to digest than pasteurized milk (27). However, a well-conducted trial in subjects with diagnosed lactose intolerance found no difference in lactose malabsorption between raw or pasteurized milk (30).

It is worth noting that independent of lactose intolerance via deficiency of the lactase enzyme, lactose is also a FODMAP, and thus symptoms associated with lactose ingestion may indicate IBS.

(Whether you have IBS or another dietary restriction, we can tailor a custom program for your needs.)

There is also a possibility that there are differences in milk tolerance between pasture and grass-fed vs. confined and ration-fed, but this remains to be studied (27). A final consideration is that fermentation of dairy may render it more digestible, as there is evidence that lactose intolerant subjects may tolerate cheeses and yogurts (31).

The fact that many people report food intolerance to commercial milk and yet report tolerance to raw milk is inconsistent with evidence from controlled trials showing no difference in symptoms between raw and commercial milk in subjects with lactose intolerance (27, 31).

Overall this suggests that many people with self-perceived dairy food intolerance are psychosomatic and not experiencing real intolerance.

Food Additives: Sulphites, Benzoates and Monosodium Glutamate

Foods additives are also commonly identified by subjects as a cause of their food intolerance symptoms, with the most common including eczema, asthma, flushing, flushing, and pain (32). However, the prevalence of food intolerance reactions to such additives is unknown (32).

Sulphites are commonly found in dried fruits, wine and cider, processed meats and package products. Food intolerance reactions to sulphites are most commonly observed in asthmatics, and a recent review noted that up to 10% of asthmatics experience symptoms from consuming sulphites (33). Sulphites also commonly result in urticaria [hives and associated rash] after ingestion (33).

Benzoates are commonly added in high concentrations to processed foods – soft drinks, sweets, ice creams, baked goods – in addition to benzoic acid naturally occurring in foods like berries (34).

Benzoates have been implicated in asthma, dermatitis, chronic urticaria, and rhinitis, however, there is limited evidence to support any direct role as most well-controlled trials show little to no effect of benzoate ingestion on the aforementioned conditions (32).

Monosodium glutamate, or MSG, is an additive used to enhance savory taste in foods. Popularised in Chinse restaurants, MSG is primarily implicated in triggering headaches. However, much the hysteria over MSG came from research in the 1960’s, and a more recent analysis of the research concluded that there is no real benefit to an MSG-free diet in subjects with chronic headaches (33).

Conclusions

 

food intolerance

 

Adult food allergy is no doubt increasing, however, there remains a significant disconnect between the prevalence of self-reported food intolerance and actual incidence rates. This isn’t discounting that someone experiences symptoms, but if you do experience symptoms of food intolerance then don’t self-diagnose.

The following checklist is a step-by-step process you can go through to help resolve any issues:

  1. Address diet quality first: increase consumption of vegetables, fruit, lean proteins, and added plant fats like nuts and olive oil, while reducing the amounts of refined flour products, baked goods, processed and packaged foods. Our coaches at IIFYM.com are here to help you improve your diet.
  2. If you seem to respond to minor amounts of wheat/gluten, then test for Coeliac first with your doctor. If that fails, then ask for serology tests for FABP2 and LBP/SCD14 – biomarkers indicative of NCWS. If that is negative, then you may have issues with FODMAPs.
  3. If you’re convinced that you respond to milk, then have your doctor perform a hydrogen breath test to determine lactose malabsorption. If you’re not lactose intolerant, but you still respond to milk and you respond to other foods like onions, leeks, garlic, then you may have issues with FODMAPs.
  4. If you suspect FODMAPS, then see an RD with a view to guiding you through the clinical low-FODMAP diet.
  5. Don’t waste your money on an IgG food “intolerance” test. All it tells you is this: you have recently consumed foods.
+ REFERENCES
  • Cianferoni, A. and Spergel, J. (2009). Food Allergy: Review, Classification and Diagnosis. Allergology International, 58(4), pp.457-466
  • Valenta, R., Hochwallner, H., Linhart, B. and Pahr, S. (2015). Food Allergies: The Basics. Gastroenterology, 148(6), pp.1120-1131.e4.
  • Verrill, L., Bruns, R. and Luccioli, S. (2015). Prevalence of self-reported food allergy in U.S. adults: 2001, 2006, and 2010. Allergy and Asthma Proceedings, 36(6), pp.458-467.
  • Stapel, S., Asero, R., Ballmer-Weber, B., Knol, E., Strobel, S., Vieths, S. and Kleine-Tebbe, J. (2008). Testing for IgG4 against foods is not recommended as a diagnostic tool: EAACI Task Force Report*. Allergy, 63(7), pp.793-796.
  • Johansson, S., Bieber, T., Dahl, R., Friedmann, P., Lanier, B., Lockey, R., Motala, C., Ortega Martell, J., Platts-Mills, T. and Ring, J. (2004). Revised nomenclature for allergy for global use: Report of the Nomenclature Review Committee of the World Allergy Organization, October 2003. Journal of Allergy and Clinical Immunology, 113(5), pp.832-836.
  • Zeng, Q., Dong, S., Wu, L., Li, H., Sun, Z., Li, J., Jiang, H., Chen, Z., Wang, Q. and Chen, W. (2013). Variable Food-Specific IgG Antibody Levels in Healthy and Symptomatic Chinese Adults. PLoS ONE, 8(1), p.e53612.
  • Kumar, V. and Wijmenga, C. (2011). Celiac disease: update from the 14th International Celiac Disease Symposium 2011. Expert Review of Gastroenterology & Hepatology, 5(6), pp.685-687.
  • Biesiekierski, J. and Iven, J. (2015). Non-coeliac gluten sensitivity: piecing the puzzle together. United European Gastroenterology Journal, 3(2), pp.160-165.
  • Uhde, M., Ajamian, M., Caio, G., De Giorgio, R., Indart, A., Green, P., Verna, E., Volta, U. and Alaedini, A. (2016). Intestinal cell damage and systemic immune activation in individuals reporting sensitivity to wheat in the absence of coeliac disease. Gut, 65(12), pp.1930-1937.
  • Biesiekierski, J., Peters, S., Newnham, E., Rosella, O., Muir, J. and Gibson, P. (2013). No Effects of Gluten in Patients With Self-Reported Non-Celiac Gluten Sensitivity After Dietary Reduction of Fermentable, Poorly Absorbed, Short-Chain Carbohydrates. Gastroenterology, 145(2), pp.320-328.e3.
  • Biesiekierski, J., Newnham, E., Irving, P., Barrett, J., Haines, M., Doecke, J., Shepherd, S., Muir, J. and Gibson, P. (2011). Gluten Causes Gastrointestinal Symptoms in Subjects Without Celiac Disease: A Double-Blind Randomized Placebo-Controlled Trial. The American Journal of Gastroenterology, 106(3), pp.508-514.
  • Barrett, J., Gearry, R., Muir, J., Irving, P., Rose, R., Rosella, O., Haines, M., Shephard, S. and Gibson, P. (2010). Dietary poorly absorbed, short-chain carbohydrates increase delivery of water and fermentable substrates to the proximal colon. Alimentary Pharmacology & Therapeutics.
  • Catassi, G., Lionetti, E., Gatti, S. and Catassi, C. (2017). The Low FODMAP Diet: Many Question Marks for a Catchy Acronym. Nutrients, 9(3), p.292.
  • Drossman, D. (2016). Functional Gastrointestinal Disorders: History, Pathophysiology, Clinical Features, and Rome IV. Gastroenterology, 150(6), pp.1262-1279.e2.
  • Jiang, X., Locke, G., Choung, R., Zinsmeister, A., Schleck, C. and Talley, N. (2008). Prevalence and risk factors for abdominal bloating and visible distention: a population-based study. Gut, 57(6), pp.756-763.
  • Lee, K. and Lee, O. (2014). Intestinal microbiota in pathophysiology and management of irritable bowel syndrome. World J Gastroenterol., 20(27), pp.8886–8897.
  • Drossman, D. and Hasler, W. (2016). Rome IV—Functional GI Disorders: Disorders of Gut-Brain Interaction. Gastroenterology, 150(6), pp.1257-1261.
  • Murray, K., Wilkinson-Smith, V., Hoad, C., Costigan, C., Cox, E., Lam, C., Marciani, L., Gowland, P. and Spiller, R. (2013). Differential Effects of FODMAPs (Fermentable Oligo-, Di-, Mono-Saccharides and Polyols) on Small and Large Intestinal Contents in Healthy Subjects Shown by MRI. The American Journal of Gastroenterology, 109(1), pp.110-119.
  • Ong, D., Mitchell, S., Barrett, J., Shepherd, S., Irving, P., Biesiekierski, J., Smith, S., Gibson, P. and Muir, J. (2010). Manipulation of dietary short chain carbohydrates alters the pattern of gas production and genesis of symptoms in irritable bowel syndrome. Journal of Gastroenterology and Hepatology, 25(8), pp.1366-1373.
  • Major, G., Pritchard, S., Murray, K., Alappadan, J., Hoad, C., Marciani, L., Gowland, P. and Spiller, R. (2017). Colon Hypersensitivity to Distension, Rather Than Excessive Gas Production, Produces Carbohydrate-Related Symptoms in Individuals With Irritable Bowel Syndrome. Gastroenterology, 152(1), pp.124-133.e2.
  • Rajilić-Stojanović, M., Jonkers, D., Salonen, A., Hanevik, K., Raes, J., Jalanka, J., de Vos, W., Manichanh, C., Golic, N., Enck, P., Philippou, E., Iraqi, F., Clarke, G., Spiller, R. and Penders, J. (2015). Intestinal Microbiota And Diet in IBS: Causes, Consequences, or Epiphenomena?. The American Journal of Gastroenterology, 110(2), pp.278-287.
  • Jalanka-Tuovinen, J., Salonen, A., Nikkilä, J., Immonen, O., Kekkonen, R., Lahti, L., Palva, A. and de Vos, W. (2011). Intestinal Microbiota in Healthy Adults: Temporal Analysis Reveals Individual and Common Core and Relation to Intestinal Symptoms. PLoS ONE, 6(7), p.e23035.
  • David, L., Maurice, C., Carmody, R., Gootenberg, D., Button, J., Wolfe, B., Ling, A., Devlin, A., Varma, Y., Fischbach, M., Biddinger, S., Dutton, R. and Turnbaugh, P. (2014). Diet rapidly and reproducibly alters the human gut microbiome. Nature, 505(7484), pp.559-563.
  • McKenzie, Y., Bowyer, R., Leach, H., Gulia, P., Horobin, J., O'Sullivan, N., Pettitt, C., Reeves, L., Seamark, L., Williams, M., Thompson, J. and Lomer, M. (2016). British Dietetic Association systematic review and evidence-based practice guidelines for the dietary management of irritable bowel syndrome in adults (2016 update). Journal of Human Nutrition and Dietetics, 29(5), pp.549-575.
  • Verhoeckx, K., Vissers, Y., Baumert, J., Faludi, R., Feys, M., Flanagan, S., Herouet-Guicheney, C., Holzhauser, T., Shimojo, R., van der Bolt, N., Wichers, H. and Kimber, I. (2015). Food processing and allergenicity. Food and Chemical Toxicology, 80, pp.223-240.
  • Suchy, F. (2010). National Institutes of Health Consensus Development Conference: Lactose Intolerance and Health. Annals of Internal Medicine, 152(12), p.792
  • Mullin, G., Belkoff, S. and Box, R. (2014). Survey to Determine Why People Drink Raw Milk. Global Advances in Health and Medicine, 3(6), pp.19-24.
  • Jianqin, S., Leiming, X., Lu, X., Yelland, G., Ni, J. and Clarke, A. (2015). Erratum to: ‘Effects of milk containing only A2 beta casein versus milk containing both A1 and A2 beta casein proteins on gastrointestinal physiology, symptoms of discomfort, and cognitive behavior of people with self-reported intolerance to traditional cows’ milk’. Nutrition Journal, 15(1).
  • Ho, S., Woodford, K., Kukuljan, S. and Pal, S. (2014). Comparative effects of A1 versus A2 beta-casein on gastrointestinal measures: a blinded randomised cross-over pilot study. European Journal of Clinical Nutrition, 68(9), pp.994-1000.
  • Mummah, S., Oelrich, B., Hope, J., Vu, Q. and Gardner, C. (2014). Effect of Raw Milk on Lactose Intolerance: A Randomized Controlled Pilot Study. The Annals of Family Medicine, 12(2), pp.134-141.
  • Williams, J., Moyle, M. and Nixon, R. (2007). Occupational contact urticaria from Parmesan cheese. Contact Dermatitis, 56(2), pp.113-114.
  • Skypala, I., Williams, M., Reeves, L., Meyer, R. and Venter, C. (2015). Sensitivity to food additives, vaso-active amines and salicylates: a review of the evidence. Clinical and Translational Allergy, 5(1).
  • Food Allergy: Adverse Reactions to Foods and Food Additives (5th edition)2015 024 Edited by Dean D. Metcalfe and others Food Allergy: Adverse Reactions to Foods and Food Additives (5th edition) Malden, MA and Oxford Wiley-Blackwell 2014 ISBN9781118744185 £149.99 $199.99. (2015). Reference Reviews, 29(1), pp.40-41.
  • Rangan, C. and Barceloux, D. (2009). Food Additives and Sensitivities. Disease-a-Month, 55(5), pp.292-311.

about the author

Alan Flanagan

Alan is a lawyer and nutritionist based in Dublin, Ireland. In addition to his legal practice, Alan is currently pursuing a Masters in Nutritional Medicine at the University of Surrey. Alan founded Align Health as an online coaching practise, and as a medium to communicate evidence-based nutrition and health science to a lay audience. From working professionals to professional athletes, Alan provides science-based solutions and protocols to guide motivated individuals to their goals. His writing can be found at alignhealth.ie


Ready To Get Started?

DISCOVER HOW TO FORCE YOUR BODY TO

TRIGGER IMMEDIATE FAT LOSS

WITHOUT GIVING UP THE FOODS YOU LOVE!

Blueprint Starter Kit

Your Custom
Macro Blueprint Starter Kit

What makes IIFYM different is that we don't force you to eat foods you hate in order to lose weight.

We actually prefer if you continue to eat the foods you love but just in the right amounts. Don't be nervous, our Custom Macro Blueprint Starter Pack shows you EXACTLY how to do it from A to Z.

OVER 25,000 CLIENTS PER YEAR

CHANGE THEIR LIVES WITH THE CUSTOM MACRO BLUEPRINT STARTER PACK

Bonus Items

As an added value, we will also include our Macro Friendly Recipe book & Ultimate IIFYM Starter Guide. That’s $34 of extra value!

$17

Free

Regular Price: $99

Sale Price: $67

$17

Free

ISN'T IT TIME YOU TRY SOMETHING

THAT'S GUARANTEED TO WORK?

Get your customized macro
blueprint starter pack now

100% Guaranteed Results or your money back! You have nothing to lose!