The Best Choice: Build Muscle, Unlock your Healthiest Self

You might have heard that muscle is also called the ‘organ of longevity’

Podcast

On 9 July 2020, I recorded a podcast with @Wildmanstrengthpt Taylor Thompson. Our discussion was mainly focused on the benefits of muscle growth, strength and power training for health, longevity and independence in old age. In that occasion, Taylor also presented his Wildman Strength & Longevity protocol for the first time. However, as we ran short of time, some topics were left uncovered, which are relevant to the process of muscle growth – such as micronutrient intakes and supplements. While you can read about, and watch the podcast here, I will attempt to give my 2 cents on what I consider to be the best hacks for muscle building in this post.

Sarcopenia and mortality

Before we dig into muscle building, it is important to understand why it is so important to our health. To do so, let’s start from the definition, and health implications of ‘sarcopenia’. The the European Working Group on Sarcopenia in Older People (EWGSOP) has defined sarcopenia as ‘the loss of muscle mass plus low muscle strength or low physical performance‘.

To asses how sarcopenia relates to human health, several studies were conducted between 2013 and 2014, in different countries and regions. What all those studies found was a strong correlation between sarcopenia and increased mortality in elderly population (80-85 years of age) (Arago-Lopera et al. 2013, Duchowny 2019, Landi et al. 2012, Landi et al. 2013). What it means, is that sarcopenia can be thought of as the direct responsible for natural mortality. Consequently, it also means that the more muscle you carry and the stronger you are, the lesser chances you have to die from sarcopenia.

Therefore, building as much muscle as possible at a young age can delay or prevent sarcopenia, hence extending one’s lifespan.

Power and independence in old age

Moreover, other studies have specifically associated strength and power training with increased functionality and independence in old age (De Vos 2008, Hazell 2007, Marsh et al. 2009). What this means, is that building significant strength and power at a young age can also extend one’s lifespan.

For these reasons, I like to refer to muscle as ’the bank of longevity’: invest in muscle now, live a better future.

How do we build muscle?

The four most important elements for muscle growth

1. Resistance training

In order to grow, muscle needs to be stimulated. Muscle growth is indeed a consequence of the body adapting to a consistent stimulus. As is of common knowledge, the highest hypertrophic response is achieved within a 8-12 rep range performed at 60-80% 1RM. However, sets of 5-6 reps can also promote hypertrophy, while building strength at the same time.

2. Leucine

This is by far the most important amino acid for muscle building, as it acts with insulin to activate the mTor pathway, which is responsible for cell metabolism and growth. To activate mTor, just as little as 2.5g of leucine are necessary, corresponding to 80-120g red meat, poultry or seafood; 17g whey protein isolate; 3 eggs; 70g hard cheese; 140g cottage cheese; 400g tofu (not very practical); 380g lentils (not very practical, either); 120g almonds (again, not very practical) (source: https://www.sportsdietitians.com.au/wp-content/uploads/2015/04/110701-Protein-Supplementation_General.pdf). While all protein-containing foods are great to build muscles, those high in leucine play the most important role in the process.

3. Carbohydrates

Although dietary carbohydrates are non essential nutrients in the human diet, meaning that the body can manufacture glucose from fat and protein (the process is known as ‘gluconeogenesis’), post exercise carbohydrate intake facilitates insulin production, activating the mTor pathway, and creating the ideal environment for muscle protein synthesis. However, highly processed carbohydrates (such as high-fructose corn syrup) can play a detrimental role in insuline sensitivity, in the long term. Therefore, try to prioritise fruit, raw honey, starches, gluten-free grains and legumes.

4. Sleep

Muscle is stimulated in the gym, nourished with adequate leucine and carbs but it is regenerated while resting. Human growth hormone (HGH), which is responsible for all growth mechanisms in the body, is indeed secreted by the anterior pituitary gland while sleeping. Adequate sleep is therefore crucial to muscle building. Furthermore, an optimised sleep-wake cycle regulates the melatonin-cortisol ratio, hence reducing stress and promoting muscle-building even more.

My favourite supplements for muscle growth

1. Pre Workout. L-Arginine

It is a precursor of nitric oxide and has two important roles, as it:

  • stimulates blood production – potentially facilitating nutrient delivery in the muscles –
  • has been shown to increase growth hormone levels in the blood.

Even though the literature on taking L-Arginine supplements is still controversial and further research is probably needed to confirm its efficacy, taking 3 g dissolved in 50ml water as a pre-workout can potentially increase both performance and muscle growth. 

2 Intra Workout. EEAA (essential amino acids)

To sustain high-volume workouts, dissolving 15g EEAA in 500ml water, with ¼ tsp Himalayan salt and 1tsp unsweetened berry jam or organic honey has become a must for me. During high volume training, glycogen stores might run low, so sipping high GI sugars (from berry jam or honey) will replenish glycogen fast, while adding EEAA will prevent further energy from being taken from muscle fibres. I also add Himalayan salt to replenish the electrolytes that get lost through sweat.

3 Post Workout. L-Glutamine and Creatine

  • Glutamine is a conditionally essential amino acid, meaning that, although it is produced by our body in otherwise sufficient amounts, in particularly stressful circumstances, the body tends to run low and it needs to be replenished. 5-10g post workout are proven to speed up recovery in some trial studies (e.g. Legault et al. 2015).
  • Creatine is a compound produced by the liver, made from the amino acids arginine, glycine and methionine. As you might know, it is also used by the muscle cells to produce energy. Therefore, ensuring that creatine stores are always full, assists muscle recovery and facilitates energy production in muscles. The debate as to whether it is advisable to assume creatine before or after a workout is still open, however I personally prefer adding 1 scoop to my post-workout whey protein shake, alongside l-glutamine.

4 Before Bed. Tryptophan

Tryptophan is a precursor of both melatonin and serotonin (the happiness hormone). Melatonin being essential for HGH production and release, drinking 3g of tryptophan with 50ml water before bed can potentially facilitate muscle growth.

Conclusion

Even though the debate is still open as to whether taking supplements can significantly improve muscle growth, research seems to unanimously agree on the health benefits of muscle mass, as well as on the functional role of strength and power training. One more caveat concerns the quality of supplements.

Indeed, the supplement industry is a relatively new one, and substantial studies on long-term supplementation lack to this day – to give an example, tryptophan was banned for well over a decade (from 1990 to 2005), as tryptophan produced by a certain company was proven to cause eosinophilia myalgia syndrome (EMS), due to toxins elicited by the genetically-modified bacteria used by that company in its fermentation process (you can read the full story here). Whether deciding to take supplements to help muscle growth is your choice – and so are the potential risks involved – you can surely control the quality of such supplements. Here are some easy tips to do so:

  • make sure you read labels carefully and avoid those with too many additives (these are usually encoded as an ‘E-numbers’ code, so you basically want to avoid as many ‘E’s as possible);
  • try to always choose the brand which contains the highest possible percentage of supplement (and the lowest of additives);
  • before purchasing supplements from an unknown brand, do some research and check if, and how many peer-reviewed studies exist on that specific product: even though such studies might be highly biased by the interests of the supplement company, reading through what some scientists have found out about a product, is always better than knowing nothing at all.

Remember, when it comes to health, make sure you always choose quality over quantity. Stay strong everyone!

Book a FREE consultation today, and learn how you can build muscle quickly and effectively:

References

Arango-Lopera, V. E et al. 2013. ‘Mortality as an adverse outcome of sarcopenia’. The journal of nutrition, health & aging17:259–262

De Vos, Nathan J. et al. 2008. ‘Effect of Power-Training Intensity on the Contribution of Force and Velocity to Peak Power in Older Adults’. Journal of Aging and Physical Activity 16(4):393-407

Duchowny, Kate. 2019. ‘Do Nationally Representative Cutpoints for Clinical Muscle Weakness Predict Mortality? Results From 9 Years of Follow-up in the Health and Retirement Study’. J Gerontol A Biol Sci Med Sci. 74(7): 1070–1075

Hazell, Tom et al. 2007. ‘Functional Benefits of Power Training for Older Adults’. Journal of Aging and Physical Activity 15(3):349–359

Landi, Francesco et al. 2012. ‘Sarcopenia and Mortality among Older Nursing Home Residents’. Journal of the American Medical Directors Association 13(2):121-126

Landi, Francesto et al. 2013. ‘Sarcopenia and mortality risk in frail older persons aged 80 years and older: results from ilSIRENTE study’. Age and Ageing 42(2):203-209

Legault, Zachary; Nicholas Bagnall and Derek S. Kimmerly. 2015. ‘The Influence of Oral L-Glutamine Supplementation on Muscle Strength Recovery and Soreness Following Unilateral Knee Extension Eccentric Exercise’. International Journal of Sport Nutrition and Exercise Metabolism 25(5):417-426. https://doi.org/10.1123/ijsnem.2014-0209

Lomonosova, Yulia N.; Boris S. Shenkman; Grigorii R. Kalamkarov; Tatiana Y. Kostrominova; Tatyana L. Nemirovskaya. 2014. ‘L-arginine Supplementation Protects Exercise Performance and Structural Integrity of Muscle Fibers after a Single Bout of Eccentric Exercise in Rats’. PLoS ONE 9(4): e94448. https://doi.org/10.1371/journal.pone.0094448

Marsh, Anthony P. et al. 2009. ‘Lower Extremity Muscle Function after Strength or Power Training in Older Adults’. Journal of Aging and Physical Activity 17(4):416–443

McConell, Glenn K. 2007. ‘Effects of L-arginine supplementation on exercise metabolism’. Current Opinion in Clinical Nutrition and Metabolic Care 10(1):46-51 doi: 10.1097/MCO.0b013e32801162fa

Further references are given in the podcast show notes.

Why Fibre Might not be as Healthy as you Think

Why fibre might not be as healthy as you think - Fitnosophy

I first started questioning the role of fibre in my diet when I was diagnosed with IBS for the first time in 2009

Back then, I was told to cut back on leafy greens, pasta, bread and gluten containing grains. I recall experiencing significant benefits within less than one week. However, due to my lifestyle at the time, I slowly reintroduced most of those foods back into my life as soon as all my symptoms went away.

When my IBS reached its apex in 2018, however, I was put on a strict low FODMAP diet by my GP, which excluded way more food groups than those listed above. After cautiously testing which ones I could reintroduce back into my diet without triggering IBS symptoms, I realised that there were still a whole lot of foods, which I would never eat in my life again, if not on very special occasions (e.g. most grains, alcohol, cherries, watermelon, apricots, mushrooms, just to name a few).

Despite what the mainstream culture seemed to promote, I found out I was better off without fibre, or with just a minimum amount of it.

What is fibre?

Technically, fibre is a subspecies of carbohydrates. Carbohydrates can be thought of as long and complex chains of simpler glucose molecules (made out of carbon, hydrogen, oxygen). Even though carbohydrates are non essential macronutrients (in fact, through a metabolic pathway known as ʻgluconeogenesisʼ, glucose molecules are manufactured in the liver from carbon substrates found in amino acids and lipids), paradoxically, they happen to be the bodyʼs preferred source of energy. Indeed, they appear to be the most accessible source of glucose, which is essential to run vital brain functions, as well as one of the muscle-skeletal energy systems.

Not all carbohydrates, however, are broken down by the body to produce energy, and here is where fibre comes into play: both soluble and insoluble fibre, along with resistant starch, present a molecular structure that our enzymes are unable to break down. The function of fibre, therefore, is not that of providing our body with energy.

Fibre can be soluble or insoluble:

  • Insoluble fibre (roughage) passes through our GI and its only function is to create stool volume.
  • Soluble fibre and resistant starch are fermented by gut bacteria and dissolved in water, forming a gel in the colon.

Both soluble and insoluble fibre have been popularised in recent years, due to their positive association with: colon cancer reduction; blood glucose reduction; LDL reduction (which might not be as a positive thing as you think, after all, but it would be off-topic now). However, all those positive associations should be rediscussed if you have a GI pathology. 

Some literature

Even though fibre (without differentiating between soluble and insoluble) was said to be effective in a small group of Chinese population (33 constipated patients and 20 healthy individuals) who underwent a 4-week kiwi fruit treatment (On On Chan et al. 2007), a causation fibre-relief from constipation is still controversial. In particular, the benefits found in the consumption of a kiwi fruit twice a day could come from water, vitamins and minerals and not necessarily from the fibre itself. A meta analysis of the existing literature from 2012 showed that ʻfiber intake can obviously increase stool frequency in patients with constipation. It does not obviously improve stool consistency, treatment success, laxative use and painful defecationʼ (Yang et al. 2012).

Two studies are worth being mentioned in this regard:

  1. An interventional study from 1997 (Voderholzer et al) investigated the role of dietary fibre in the treatment of chronic constipation. What was found was a positive outcome in patients with no GI issues, whereas no significant change was seen in the other group: ʻEighty percent of patients with slow transit and 63% of patients with a disorder of defecation did not respond to dietary fiber treatment, whereas 85% of patients without a pathological finding improved or became symptom freeʼ. So, they concluded ʻSlow GI transit and/or a disorder of defecation may explain a poor outcome of dietary fiber therapy in patients with chronic constipationʼ.
  2. A more recent study from 2012 (Kok-Sun et al) investigated the role of fibre in idiopathic constipation and found no benefits in introducing fibre in the diet. In fact, ʻpatients who stopped or reduced dietary fiber had significant improvement in their symptoms while those who continued on a high fiber diet had no changeʼ. So, the authors conclude, ʻidiopathic constipation and its associated symptoms can be effectively reduced by stopping or even lowering the intake of dietary fiberʼ.

Further Reflections

Gut Dysbiosis

One more thing to be considered is the dysbiosis (microbial imbalance) characterising IBS sufferers and its relation to the efficacy of a low FODMAP diet: according to the most recent hypothesis on IBS, most of the symptoms appear to be triggered by an excess of bacteria in the colon, that can be overfed, when too many prebiotics are ingested, leading to an excess of fermentation, and, therefore, gas and pain (see Lyra and Lahtinen 2012, Collins 2014, Simrén 2014, Shukla et al. 2015, Putignani et a. 2016, Benno et al. 2016, Principi et al. 2018, ).

High FODMAP foods, by definition, are fermentable sugars: some of them (mono and disaccharides) are very small molecules, others are bigger polymers (e.g. polyols), others are long glucose polymers, known as polysaccharides. Fibre and starch are also polysaccharides, which makes it easy to understand why many fibrous or starchy foods also happen to be high FODMAP. However not all polysaccharides are highly fermentable, and nor are all other mono and disaccharides, which explains why some fibrous foods are still tolerated by IBS sufferers.

Soluble and Insoluble Fibre and IBS

Moreover, the tolerance level is individual and depends upon each individual’s unique microbiome. Consuming soluble fibre and resistant starch will obviously increase the chance of the bacteria being overfed, even within the recommended intake for average population.

Consuming insoluble fibre might also aggravate IBS symptoms. Indeed, due to the impaired fermentation in the colon, also the stool transit appears impaired: in so called ‘IBS-D’ (IBS-diarrhoea) sufferers, excess water is drawn and bowel movements are accelerated; by contrast, in so called ‘IBS-C’ (IBS-constipation) sufferers, bowel movements are slowed down. Ingesting a bulking, such as insoluble fibre, might potentially interfere with the transit, especially in the case of IBS-C sufferers, as happened in the populations of the constipation studies discussed above.

SIBO, IBD and Other Conditions

A similar discourse could surely be done in regard to SIBO (Small Intestinal Bacterial Overgrowth), which differs from IBS in that the overgrowth appears to be localised predominantly in the small intestine (it is possible that someone with IBS is also affected by SIBO, whereas someone affected by SIBO might not experience IBS symptoms). In that case, fermentation might occur in the small intestine, at the stage of absorption and assimilation of nutrients, which would in turn be impaired even more by the excess of bacterial population.

Lastly, also IBD (Inflammatory Bowl Disease), an umbrella term describing Crohn’s disease and ulcerative colitis also appears to be characterised by dysbiosis (see Putignani et a. 2016) and therefore might be impaired by a diet high in fibre.

Conclusion

Including both soluble and insoluble fibre in the diet of a healthy individual, with no GI issues, is not only harmless but even beneficial. In the case of IBS, SIBO or IBD sufferers, however, an overconsumption of fibre might aggravate some of the symptoms.

These days we find ourselves surrounded with all kinds of diets and lifestyles, each of them advocating to be ‘the best one’ and/or ‘the most suitable for humans’. Even celebrities popularise certain diets or lifestyles, and other ‘gurus’ claim tons of scientific evidence behind what they promote. It’s important, instead, to understand that not every diet or lifestyle can be suitable for everyone.

To cut a long story short, before jumping into a fad diet, or before making any relevant dietary intervention, please, do your own research and seek professional help.

Need simple, gut-friendly recipes?

My recipes are all low-FODMAP and gut friendly. Make sure you check them out!

References

Benno, Peter; Dahlgren, Atti-La, Befrits, Ragnar, Norin, E., Hellström, P. M., & Midtvedt, T. 2016 . ‘From IBS to DBS: The Dysbiotic Bowel Syndrome’. . Journal of Investigative Medicine High Impact Case Reportshttps://doi.org/10.1177/2324709616648458

Botschuijver, Sara; Guus Roeselers; Evgeni Levin; Daisy M.Jonkers; Olaf Welting; Sigrid E.M. Heinsbroek; Heleen H. de Weerd; Teun Boekhout; Matteo Fornai; Ad A.Masclee; Frank H.J. Schuren; Wouter J.de Jonge; Jurgen Seppen; René M.van den Wijngaard. 2017. ‘Intestinal Fungal Dysbiosis Is Associated With Visceral Hypersensitivity in Patients With Irritable Bowel Syndrome and Rats’. Gastroenterology 153(4): 1026-1039. https://doi.org/10.1053/j.gastro.2017.06.004

Collins, Stephen M. 2014. ‘A Role for the Gut Microbiota in IBS’. Nature Review Gastroenterology Hepatology 11497–505. https://doi.org/10.1038/nrgastro.2014.40

Lyra, Anna and Sampo Lahtinen. 2012. ‘Dysbiosis of the Intestinal Microbiota in IBS’. In Godfrey Lule (ed.). Current Concepts in Colonic Disorders. Rijeka (Croatia): InTech:261-276.

Yang, Jing; Hai-Peng Wang; Li Zhou; and Chun-Fang Xu. 2012. ʻEffect of dietary fiber on constipation: A meta analysisʼ. World Journal of Gastroenterology 18(48):7378–7383. doi: 10.3748/wjg.v18.i48.7378

Kok-Sun Ho; Charmaine You Mei Tan; Muhd Ashik Mohd Daud; and Francis Seow-Choen. 2012 ʻStopping or reducing dietary fiber intake reduces constipation and its associated symptomsʼ. World Journal of Gastroenterology 18(33):4593–4596. doi: 10.3748/wjg.v18.i33.4593

On On Chan, Annie; Gigi Leung; Teresa Tong; and Nina YH Wong. 2007. ʻIncreasing dietary fiber intake in terms of kiwifruit improves constipation in Chinese patientsʼ. World Journal of Gastroenterology 13(35):4771–4775. doi: 10.3748/wjg.v13.i35.4771

Principi, Nicola; Rita Cozzali; Edoardo Farinelli; Andrea Brusaferro; Susanna Esposito. 2018. ‘Gut dysbiosis and irritable bowel syndrome: The potential role of probiotics’. Journal of Infection 76(2): 111-120. https://doi.org/10.1016/j.jinf.2017.12.013

Putignani, Lorenza; Federica Del Chierico; Pamela Vernocchi; Michele Cicala; Salvatore Cucchiara; Bruno Dallapiccola. 2016. ‘Gut Microbiota Dysbiosis as Risk and Premorbid Factors of IBD and IBS Along the Childhood–Adulthood Transition’. Inflammatory Bowel Diseases 22(2):487-504. https://doi.org/10.1097/MIB.0000000000000602

Simrén, Magnus. 2014. ‘IBS with intestinal microbial dysbiosis: a new and clinically relevant subgroup?’ Gut http://dx.doi.org/10.1136/gutjnl-2013-306434

Shukla, Ratnakar; Ujjala Ghoshal; Tapan N. Dhole; Uday C. Ghoshal. 2015. Fecal Microbiota in Patients with Irritable Bowel Syndrome Compared with Healthy Controls Using Real-Time Polymerase Chain Reaction: An Evidence of Dysbiosis’. Dig Dis Sci 60:2953–2962. https://doi.org/10.1007/s10620-015-3607-y

Voderholzer, Winfried A.; Schatke, Winfried; Mühldorfer, Birgit E.; Klauser, Andreas G.; Birkner, Berndt; Müller-Lissner, Stefan A. 1997. ʻClinical Response to Dietary Fiber Treatment of Chronic Constipationʼ. American Journal of Gastroenterology 92 (1):95-98

Is Keto a Powerful Lifestyle? Free Life Advice

Fitnosophy - Keto

My 6-Month Experiment

My Reasons, Motivations and Expectations

After quitting veganism in April 2019, I started experimenting with a ketogenic diet, to see if I could: 1) fix my digestion, 2) improve my performance at the gym, 3) burn some body fat more easily. I was also curious to understand what kind of impact it might have on my energy levels and overall focus. I officially began my experiment the last week on May, and concluded it at the end of November.

My Protocol

As I was expecting (based on the literature I had read and the video I had watched), the first couple of weeks were the toughest ones. The principle of ketosis is that, instead of using glucose from carbs as your primary source of energy, your liver produces ketone bodies from short-chain fatty acids (SCFA) which travel across your body and supply energy to organs and tissues (thus sparing glucose supplies for your brain — as it can’t work without). Shifting from carbs to fats can take some time and can cause brain fog, lack of energy, headache (the so-called ‘keto flu’). So, as you can imagine, the first couple of weeks can be very painful. To reach ketosis and stay in it, all you need to do is:

  • Fast until you’ve depleted all of your glycogen stores
  • Consume a diet high in fats (60-75% of your calories), moderate in proteins (20-30% of your calories), and very low in carbs (5-10% of your calories, usually coming from low GI vegetables and fruit, such as cruciferous veggies, green beans, lettuce, peppers, tomatoes, berries etc.)
  • Avoid high GI foods (starch, grains, most fruit, sugar, syrup, honey, etc.)
  • Limit your daily meals to 2-3, as you don’t want your insuline to spike, or it’ll prevent lipolysis (the process of fatty acids being released from the adipose cells to be used for energy).

As I work out everyday, and as I like to keep my workouts’ volume quite high, I adjusted my macros so that my carbs would never go below 50g a day, to be split between pre- and post-workout meals (what is commonly called a ‘modified or targeted ketogenic diet’). So my typical day looked like this:

  • 4-6:30 am. Breakfast: water and lemon, coffee, peppermint tea
  • 10-11am. Lunch: 3 duck eggs, butter, rocket leaves, sardines or mackerel, anchovies
  • 2-3pm. Pre-workout shake: whey isolate 97% protein powder, 1 small green banana or 1 cup of grapes
  • 6pm. Dinner: salmon/lamb mince/beef mince/steak/liver/kidneys/lamb heart cooked in butter or coconut oil, steamed or baked vegetables (courgettes, aubergines, tomatoes, bell peppers, spinach, green beans), coconut yoghurt with frozen berries, 100% dark chocolate.

My Results

As I’ve anticipated, the first 2 weeks were really tough and my performance at the gym suffered quite a bit. Due to the lack of glycogen in my muscles, I couldn’t cope with high volume training, so I decided to lower my rep range and increase the weight (this way I could solely rely on the phosphocreatine energy system, in which ATP is more efficiently replenished than in the lactic acid energy system). Once in ketosis and fully adapted to using fats, however, I was able go back to my usual workout routine for most exercises. As the body becomes more efficient at using fats, indeed, the process of gluconeogenesis (namely the production of glucose out of fats and amino acids) also becomes smoother and glycogen can be stored in muscles just as easily as when running on carbs. However, I never managed to go back to my usual range of reps in exercises such as hack squats and pull-ups, in which the demand for glycogen is too great for the tiny amount produced by my liver and kidneys from other macronutrients. According to some studies on rats (Fournier et al. 2002) and on humans (Fournier et al. 2004), glycogen can be replenished even in the absence of food. However, it also depends on genetic predisposition, and, at this point, I think my body is not as genetically efficient at producing glycogen as someone else’s.

The other aspect I wanted to scrutinise was my digestion. Although I was on a low FODMAP version of a ketogenic diet, the high amount of fats would occasionally get me bloated and slightly constipated. However, my energy levels were always high (after the first couple of weeks), and my appetite significantly decreased (as I wasn’t relying on insulin anymore). This subsequently improved my focus and my sense of balance and stability.

Surprisingly, although most people go keto because it is one of the most effective ways to lose weight, I must admit that the aesthetic effects of the diet is the only aspect of my experiment that has disappointed me. Regardless of what the literature says, my muscles never seemed to be fully replenished with glycogen and would appear flat most of the time (as I said, it might be that my genetics is not really efficient at producing glycogen). Moreover, even though staying in ketosis can be an excellent way to lose fat, it makes it really hard to gain weight. When I started my usual bulking after summer, I found it really difficult to put on weight beyond my maintenance. For this reason, at the end of November, I decided to go back to my typical 5-6 meals a day, increasing my carbs and lowering my fats until next spring (at least).

My Advice for You

Overall, I’ve become more efficient at using fats and much less sensitive to blood sugar fluctuations. Moreover, increasing the amount of fats also increases the amount of fat-soluble vitamins (A, D, E, K) that can be absorbed and can be beneficial for your health. For both these reasons, I would encourage everyone to try. Here’re my tips and strategies if you’re interested in trying:

  • Set a realistic timeframe for results to occur (at least 8-12 weeks) and be mentally prepared for the first 2-3 weeks being extremely tough
  • Plan your meals and shopping list in advance: although most keto recipes are very easy to make, you might not be used to cooking with butter and eating fatty cuts of meat or fish, or, in the initial phase, you might have some sugar cravings that you might want to satisfy the ‘sugar-free way’ (there’re plenty of keto-friendly dessert recipes online and many require just a few ingredients). The further you go with your diet, however, the less cravings you’ll have
  • Make sure you eat enough calories (i.e. make sure you replace the calories you’re taking away from carbs with the same amount coming from fats). The rule of thumb is this: 1g of fat has slightly more than twice the amount of calories of 1g of carb. Therefore 50g of pasta or rice can be easily replaced with 20-25g of butter or hard cheese, to give an example
  • Make sure you keep your diet varied and never boring. Try to learn 1 new recipe every week using 1 different low GI vegetable and 1 different fatty cut of meat or fish. You’ll be surprised by how delicious such recipes can be!
  • Enjoy the process and don’t be too hard on yourself if you cheat from time to time. Remember to embrace the growth and the wisdom that experimenting with a new lifestyle will bring you but keep it fun, easy and realistic!

If you’ve liked this post, stay tune because I’m planning to share some ‘guilt-free’ keto recipes for delicious cakes or desserts. 🙂

References

Fournier PA, Bräu L, Ferreira LD, Fairchild T, Raja G, James A, Palmer TN. 2002. ‘Glycogen resynthesis in the absence of food ingestion during recovery from moderate or high intensity physical activity: novel insights from rat and human studies’. Comparative biochemistry and physiology. Part A, Molecular & integrative physiology (Nov)133(3):755-63 (DOI: 10.1016/s1095-6433(02)00254-4).

Fournier PA, Fairchild TJ, Ferreira LD, Bräu L. 2004. ‘Post-exercise muscle glycogen repletion in the extreme: effect of food absence and active recovery’. Journal of sports science & medicine (Sep)1;3(3):139-46.