There is no definitive answer to what the most optimal diet looks like, so each will largely depend on personal preference. With this in mind, individuals can still make lifestyle changes to accommodate their diet and fitness goals.
Practicing moderation will become key in any lifestyle looking for balance. This means being able to show restraint and be mindful while enjoying the foods you love.
If having something sweet or say having dessert every night is something you currently do, you can modify this by restricting desserts or sweets to 3x a week or even just on weekends. Essentially, the goal would be to live in an 80/20 rule. 80% of the foods you eat are whole and nutrient densewhile 20% is for those times where you need that wiggle room whether it be to curb cravings, enjoy a night out with the girls or guys, and any other occasion where you may be faced with options that include sugar.
Don’t try to cut out sugar cold turkey all at once. As we said, moderation is key. Before you know it you’ve gone a week without a fix and then on the last day, you house an entire king-sized Hershey bar at once, sending your blood glucose and insulin levels through the roof.
Do track and pay attention to what you are eating. Get blood work done. Or if you are really into the nerdy stuff, buy a glucometer and strips and see where your blood sugar is at from time to time. Anecdotally, I have known many people to not even know they were pre-diabetic until they started looking at their blood glucose levels. Imagine if they didn’t know, continued their same habits, only to find themselves with Type 2 diabetes down the road? No, thanks!
Don’t deprive yourself to the point of a binge. Everyone is different. Some people can go most of the year with only indulging a handful of times, while others reach for a pop tart or ice cream weekly, or even daily.
Remember, context is key, everyone has different host factors and what may be unhealthy for you may not be for someone else. We hope you enjoyed this 3 part series on sugar! Feel free to reach out to us on Instagram or at email@example.com and let us know what you think!
Previously in part 1 of our series, Gillian discussed how sugar and HFCS won’t to kill you, in a specific context. But in what context is sugar and HFCS actually toxic? In this part of the series, we will take a deep dive into the metabolic impact of the sugar and HFCS.
Before we get into the nitty-gritty, let’s go ahead and define the context of toxic. First things first, let’s clarify our semantics. Many people make definitive statements without full understanding.
According to Harrison’s Principles of Internal Medicine:
Toxicity: The degree to which a substance and harm humans or animals
Acute Toxicity: involves harmful effects in an organism through a single or short-term exposure.
Subchronic Toxicity: The ability of a toxic substance or mixture of substances to cause effects for more than 1 year but less than an entire lifetime of the organism.
Chronic Toxicity: The ability of a substance or mixture of substances to cause harmful effects over an extended period, usually upon repeated or continuous exposure, sometimes lasting the entire life of the organism.
As you can see, the word toxic can be subdivided into the 3 aforementioned categories based on how long/often a substance is exposed and how long it takes to cause insult. Therefore, it is important that we make this clear: Acute toxicity is NOT the same as chronic toxicity.
It is also important to consider that there is a statistical distribution of toxicity of substances to subject. Let’s take alcohol for example. Some people may have 2 drinks before they begin to feel drunk, and others may not be phased by 5. In short, there is a spectrum of susceptibility to any toxin.
What we want to shed light on here is how we get to chronic toxicity, right? When we have too much sugar too often, what happens?
Well going back to our alcohol example, it is important to remember that what we do eat, and drink is cumulative. Even taking in alcohol in smaller doses repeatedly speeds up the aging process, disrupts neural pathways, leads to cardiomyopathy (stretching and dropping of the heart muscle), arrhythmias, high blood pressure, fatty liver disease, pancreatitis, cancer, aaaand you get my point… Which is this: just because a dose doesn’t result in acute toxicity immediately doesn’t mean that it can’t or won’t result in chronic toxicity.
It has been both researched and argued that sugar is a unique macromolecule, distinct from other carbohydrates. Studies have shown that sugar is not “just” an empty calorie. Many arguments have been made that the toxicity of sugar is related to itshepatic (liver) metabolism. Specifically, in excess (another context word), fructose increases VLDL production (very low-density lipoprotein), which carry triglycerides (a type of fat) to your tissues. Which in turn increases apoB (an important component of many lipoproteins that are involved in atherosclerosis and cardiovascular disease) or LDL-P due to carrying more triglycerides. Mechanistic studies suggest that cardiovascular disease and metabolic syndrome result from the rapid hepatic metabolism of fructose catalyzed by a specific enzyme that generates a precursor for de novo lipogenesis (making of new fat) and leads to increased uric acid levels (which can lead to gout). Research also shows that at reasonable doses, insulin resistance is worsened which amplifies the harm that other foods may have on your body.
Like many topics in the fitness industry, there are debates on ideas in the world of scientific research. But even those who don’t subscribe to the camp of sugar being metabolically significant, some argue that fructose consumptions may impact subsequent food consumption in a way that plain glucose doesn’t. We can probably stand by this from an anecdotal standpoint as well. When we eat sugar, we may not feel satiated or may crave even more food, which serves as a decent Segway into my next point: that there is emerging research to show that sugar is addictive. Even in ways comparable to heroin or cocaine as suggested by MRI. So even if you don’t buy that sugar is harmful, it may make you eat more which we saw from Gillian’s article can be the harm in itself.
If your and APOE4 allele carrier like me (a gene that increases your risk for Alzheimer’s and dementia), then controlling sugar consumption is imperative in this respect. This will have to be an article for another day, but long story short: someone who is predisposed to Alzheimer’s, dementia, or any other early onset of cognitive decline has to spare the glucose metabolism of their brain in order to try and conserve optimal cognition. Eating too much sugar may speed up the onset of cognitive decline if you are not careful (let us know if you’d like an article that dives deep into the neurological effect of food!)
Laid out for you are a few different points as to how sugar can be harmful, but what we haven’t really gotten into is dose, and at the end of the day it’s the dose that kills you not the drug. Therefore asking “is sugar toxic” becomes a dumb question. It’s the same thing as me asking “is water toxic?” or “is oxygen toxic?”. YES, water and oxygen can be lethal at extremely high doses. I mean, still appreciate that they are essential to life, but know that too much of anything is bad for you.
Circling back to Laurin’s intro, context is key. Luckily, there are amazing researchers that have considered host factors, genetic predispositions, etc. and that sometime in the near future we can have a definitive answer on what does hurts who. Tune in TOMORROW for Part 3, where we discuss the “happy medium” and practical applications for you!
Stanhope, K. L., Schwarz, J. M., & Havel, P. J. (2013). Adverse metabolic effects of dietary fructose: results from recent epidemiological, clinical, and mechanistic studies. Current Opinion in Lipidology, 24(3), 198.
Zimmerman, H. J. (1999). Hepatotoxicity: the adverse effects of drugs and other chemicals on the liver. Lippincott Williams & Wilkins.
Stanhope, K. L. (2012). Role of fructose-containing sugars in the epidemics of obesity and metabolic syndrome. Annual review of medicine, 63, 329-343.
Stanhope, K. L., Bremer, A. A., Medici, V., Nakajima, K., Ito, Y., Nakano, T., … & Keim, N. L. (2011). Consumption of fructose and high fructose corn syrup increase postprandial triglycerides, LDL-cholesterol, and apolipoprotein-B in young men and women. The Journal of Clinical Endocrinology & Metabolism, 96(10), E1596-E1605.
Attia, Peter. “Is Sugar Toxic?” The Nerd Safari, 2013 blog, Link to post (www.peterattiamd.com/is-sugar-toxic/).
HFCS Image: By Jü – Own work, CC0, https://commons.wikimedia.org/w/index.php?curid=15407275
The debate about sugar is all around us. Everywhere you look. First, it’s fine, then it’s god awful, then it’s not the worst thing ever? There is a lot of controversy in the media, which generally offers garbage advice, but even within the scientific community, there are PRO and ANTI sugar camps. What sugar (and most everything, actually) boils down to is context. Context is king.
In our three-part series, assistant coach Gillian and admin Karina debunk all things sugar. In the first part of this series, Gillian covers the sugar and high fructose corn syrup myth and drives home the message of overall calorie balance and moderation, cited with research. But what happens when calorie balance and context are lost?
In the second part of the series, Karina dives into how chronically high levels of sugar intake coupled with lifestyle factors may become toxic, leading many to find themselves with metabolic disease. Lastly, they sum it up in a practical article detailing lifestyle modifications and a ‘do’s and don’ts cheat sheet’ per se on how to optimize health, longevity and physique goals while also enjoying some treats. Because#treatyoself
– Laurin Conlin, Founder and coach | @laurinconlin
Some of our country’s biggest issues concern weight gain and the rapid decline of our health. Not surprisingly, the way that our media has promoted weight loss methods and myths to the public is not ideal. You’ve most likely seen magazines at the checkout line with new headlines each week about the ‘secret’ to weight loss. These ‘fat-blasting’ diets keep popping up and most that are popularized is greatly due to how they are praised or demonized in our media. Fad diets promoted through fear tactics (fears that ‘x’ makes us fat) set many up for failure.
No part of the diet has gone without some kind of negative backlash from consumers. First carbs make you fat, then fat makes you fat, and the list goes on… More recently, sugar has been labeled one of the worst things for our health. Specifically, high fructose corn syrup (HFCS) has received possibly the worst reputation in the past few years. Look anywhere, and you’ll find plenty of sources that claim that sugar will kill you. I know; it seems a bit intense but remember contest is key. However (thankfully), research has helped clear the air on the relationship between sugar, HFCS and weight gain.
If you aren’t familiar with the debate around HFCS, the American Journal of Clinical Nutrition published an article in 2004 with the intention of stirring up controversy. Bray and others made the claim that our increased use of HFCS in beverages mirrors our increase in obesity, concluding that the rise in HFCS consumption plays a key role in the obesity epidemic. The authors mention how drinks sweetened with sugar were linked with higher caloric intake and weight gain. What they failed to consider here was that the total caloric intake would be the main culprit, and instead pointed at HFCS as the main factor causing obesity. (1) This is problematic in that we cannot claim the presence of cause and effect here. The addition of HFCS in more processed foods and beverages in the past few decades have to lead us to consume more calories, which can then be correlated with weight gain. Added sugars are in a majority of foods, and can be easily overeaten if we are not mindful. Correlation does not always equal causation, especially if we are looking at the obesity epidemic.
Since this 2004 publication, many studies have been conducted exploring HFCS and sucrose (table sugar), the sweetener it was intended to replace. Many sought to determine if there is truly something distinctively unsafe or different about HFCS. An article from White and colleagues (2010) examined the dispute on high fructose corn syrup and found that metabolically speaking, HFCS and sucrose are basically identical (including their absorption, taste, and calories). (2) More importantly, White and colleagues point out a bigger argument concerning the obesity epidemic. There is a greater picture to look at regarding obesity; it has been able to grow through many factors (socioeconomically, environmentally, culturally, etc.) that need to be considered. The general population is certainly eating more HFCS-containing foods, but they are also eating more of everything else as well while moving less.. This has become an environment set up to promote weight gain. (2) We have yet to even think about the rest of this multifactorial epidemic.
Another noteworthy study comes from Lowndes and colleagues (2012) where their goal was to explore HFCS and sucrose and the effects on body composition and weight loss. These researchers took overweight and obese individuals, put them on weight-loss diets, and split them into 5 groups: HFCS 10%, HFCS 20%, Suc 10%, Suc 20%, and a control group. Percentages being used here reflected what percentage of the subject’s daily calories would come from the assigned sweetener. At the end of this study, researchers concluded that the levels of added sugars didn’t prevent any weight loss and body composition improvements in participants when they followed the weight loss regimen provided to them. There was also nothing noteworthy or special about HFCS that would inherently lead to weight gain. (3)
Anything in excess is not going to be good for us, so practicing moderation is key for any healthy diet. Ideally, we wouldn’t want a majority of our diet to be comprised of one nutrient and instead have a balanced mix of nutrient-dense foods, with some ‘fun’ stuff now and again. It is very unlikely that one part of the diet would be the primary cause of obesity since the root of obesity is quite complex in nature. Regardless of the caloric sweetener we use, they all still have calories and should be used mindfully in conjunction with a healthy lifestyle. Lowndes and others have presented us with a prime example of how one’s total caloric intake is most important when it exclusively comes down to weight loss and weight gain.
To conclude, the argument linking HFCS to obesity is due to a large misunderstanding. There is absolutely no need to exclude or be fearful of any food group or nutrient if you are not predisposed to any disorders in regulating blood sugar or metabolic disease. Like anything, it’s important to be wary of the health information we receive on a daily basis and to question them. Thankfully, many studies have debunked these claims and have established that a small aspect of the diet cannot be solely responsible for weight gain or obesity. Weight loss and weight gain largely come down to the total calories you consume versus the calories you expend. With this in mind, it’s important for us to keep healthy lifestyle habits in the forefront and to practice moderation alongside those bigger changes.
– Gillian SanFilippo, Team LoCoFit Coach | @gilliansanfilippo
Food has often been seen as a means of energy, macros to hit or just plain things we eat, break down, and use to build muscle and recover from training. Let’s change the lens for which we currently see food as just being a source of energy to highlight foods ability to prevent against disease and dysfunction.
It is an exciting time for the field of neuroscience, as the past 5 years have revealed evidence of the influence of our diet on the integrity of brain function and cognition. But before we get into the exciting stuff, lets define a few key terms and concepts that will be important to know:
Cognition: Mental processes that include thinking, learning, perceiving, and remembering.
Synapse: A junction between two nerve cells that allows a signal to pass from one neuron to the next.
Synaptic Plasticity: The ability of synapses to strengthen or weaken over time in response to increases or decreases in their activity.
Brain Derived Neurotrophic Factor (BDNF): A protein that induces survival, development and function of neurons.
Animal Models: On average, the protein-coding regions of the mouse and human genomes are 85 percent identical; some genes are 99 percent identical while others are only 60 percent identical. (1) Due to similarity in genomes, we can understand why human and animals suffer from a lot of the same diseases such as cancer, atherosclerosis, and neurodegenerative diseases. This is not to say that mice, rodents, drosophila flies, rabbits, and other animals used in researched are an exact model, but they do allow scientists to make implications on what treatments may or may not work in humans. We often have to test a hypothesis treatment in animals multiple times before humans can even be brought into clinical trials.
I’ll start of by saying that this will be much shorter and more summarized than I’d like it to be, but this email would be about 20 pages long if I went into the deep details, so I have provided a list of sources at the end of this email in case you really want to go down the rabbit hole!
Diet and exercise play a crucial role in shaping the brains cognitive capacity. Our brains have evolved alongside food-derived signals that influence energy metabolism and synaptic function (communicative signals between nerve cells). This can be implied by looking at skull sizes from thousands of years ago. The size of an Australopithecus man-ape skull from 2-3 million years ago, is much smaller than the modern day homo sapien skull we find in cadavers today. Therefore, we see that humans brains have evolved with access to more food. (2)
Feeding Effect on Emotion and Cognition
We can probably attest from an anecdotal standpoint the effect of food on cognition and emotion. We’ve all felt that “hangry” state where literally everything and everyone is dead to us until we get our dang food. Before we even begin eating, all it takes is the sensory inputs of sight and smell of food to affect our emotional status.
Food also triggers peptides and hormones like insulin, leptin, ghrelin, glucagon-like peptide which all serve as visceral signals that can modulate cognition and body physiology through the hypothalamic-pituitary axis (HPA). The vagus nerve which originates at the brain and innervates the gut, sending neurotransmitters both ways, and enables gut activity to influence emotions and cognition. Overall, evidence seems to show that the 2 main ways food can affects cognition is through the neural pathways through the vagus nerve and the release of certain gut peptides into our bloodstream. (2).
Vagus Nerve – Mental Health is Gut Health, Olive Retreat Blog. October 11, 2018
Your brain requires A LOT of energy, relative to the rest of your body. So you can imagine that the energy transfer from foods to your brain cells is fundamental to its function and WHAT we feed ourselves is important for this reason. Quality of synaptic function can either insult or enhance metabolic energy of the brain. BDNF is a protein that serves as a great example of how molecules can affect both energy metabolism and synaptic function(3). We can find this protein in areas of the brain that are associated with cognitive and metabolic regulation(main). BDNF can also influence appetite suppression (4,5), insulin sensitivity, and glucose(6) and fat metabolism(7).
Now let’s talk nutrients…
This one may be beating a dead horse but we have all heard a time or 10 of how important getting our omegas in is for our brain. You can typically find our instagram foodie hash-tagging #brainfood when posting pictures of things like certain fish, salmon, and avocados.
Dietary deficiency of omega-3 fatty acids in humans has been associated with increased risk of several mental disorders, including ADHD, dyslexia, dementia, depression, bipolar disorder and schizophrenia, (2,8–12).
The Omega 3 fatty acid DHA is a particularly important component of the cell membrane, but our body’s are fairly inefficient at making DHA for itself, so we are reliant on dietary DHA. Dietary supplementation of DHA has been found to elevate levels of hippocampal BDNF. DHA might also act through its effects on metabolism, as DHA stimulates glucose utilization (13) and mitochondrial function(14), reducing oxidative stress.
For the sake of context, I will also mention that in rodent studies the effects of obesogenic foods, characterized by high contents of fat and sucrose, have shown a decline in cognitive performance and reduced levels of BDNF after only 3 weeks of consuming an obesogenic diet (15). These findings suggest that the diet had a direct effect on neurons that was independent of insulin resistance or obesity.
Folate and folic acid – AKA most of your green veggies
Folate or folic acid is found in various foods, including spinach, oranges and yeast. Adequate amounts of folate are essential for brain function, and folate deficiency can lead to neurological disorders, such as depression(15) and cognitive impairment. Folate supplementation either by itself (16,17) or in conjunction with other B vitamins (18,19) has been shown to be effective at preventing cognitive decline and dementia during aging (20). It is also worth the mention that a recent randomized clinical trial has shown that a 3-year folic acid supplementation can help to reduce the age-related decline in cognitive function.
Due to the fact that the brain has such a high metabolic load, it is very susceptible to oxidative stress or the imbalance of the production of free radicals (harmful) and the body’s ability to detoxify itself from them. ANTI oxidants are compounds that help to keep this balance and mitigate high levels of free radicals. Berries, for example, have been shown to have strong antioxidant capacity through the polyphenols they contain.
Alpha lipoic acid, which is found in meats such as kidney, heart and liver, and vegetables such as spinach, broccoli and potatoes, is a coenzyme that is important for maintaining energy homeostasis in mitochondria (21). Alpha lipoic acid has been shown to reduce cognitive decay in a small group of patients with Alzheimer’s disease (22). Vitamin E, has also been implicated in cognitive performance, as low levels of vitamin E were associated with poor memory performance in older individuals (23).
Curcumin is a strong antioxidant that seems to protect the brain from lipid degradation (24) and other free radicals (25).
The table below is a short list of nutrients and their effect on the brain, as well as their food sources.
Table 1 – Brain Foods: the effect of nutrients on the brain (2)
This very short and rather “watered down” synopsis on the numerous studies that have been done looking at foods affect on the brain hopefully points to the fact that not only quantity but quality of food plays a major role in our body’s ability to utilize micronutrients to either hurt or help the healthspan of our brain and cognitive abilities. Micronutrient rich foods provide your metabolism with many more tools to reduce oxidative stress and maintain overall health than something that was 90% sucrose. While having certain foods in moderation can be key to adhering to an overall whole food/nutrient dense diet, it is important to remember that macronutrient quality affects micronutrient availability.
Thanks for reading! We hope you learned a thing or two about how to better feed your biology!
– Karina at Team LoCoFit
National Human Genome Research Institute (NHGRI). (2019). Importance of Mouse Genome. [online] Available at: https://www.genome.gov/10001345/importance-of-mouse-genome/ [Accessed 15 Feb. 2019].
Gómez-Pinilla, F. (2008). Brain foods: the effects of nutrients on brain function. Nature reviews neuroscience, 9(7), 568.
Vaynman S, Ying Z, Wu A, Gomez-Pinilla F. Coupling energy metabolism with a mechanism to support brain-derived neurotrophic factor-mediated synaptic plasticity. Neuroscience. 2006;139:1221–1234. [PubMed]
Lyons WE, et al. Brain-derived neurotrophic factor-deficient mice develop aggressiveness and hyperphagia in conjunction with brain serotonergic abnormalities. Proc Natl Acad Sci USA. 1999;96:15239–15244. [PMC free article] [PubMed]
Tonra JR, et al. Brain-derived neurotrophic factor improves blood glucose control and alleviates fasting hyperglycemia in C57BLKS-Leprdb/leprdb mice. Diabetes. 1999;48:588–594. [PubMed]
Tsuchida A, et al. Brain-derived neurotrophic factor ameliorates lipid metabolism in diabetic mice. Diabetes Obes Metab. 2002;4:262–269. [PubMed]
Adams PB, Lawson S, Sanigorski A, Sinclair AJ. Arachidonic acid to eicosapentaenoic acid ratio in blood correlates positively with clinical symptoms of depression. Lipids. 1996;31 (Suppl):157–161.[PubMed]
Peet M, Laugharne JD, Mellor J, Ramchand CN. Essential fatty acid deficiency in erythrocyte membranes from chronic schizophrenic patients, and the clinical effects of dietary supplementation. Prostaglandins Leukot Essent Fatty Acids. 1996;55:71–75. [PubMed]
Hibbeln JR. Fish consumption and major depression. Lancet. 1998;351:1213. [PubMed]
Horrobin DF. Schizophrenia: the illness that made us human. Med Hypotheses. 1998;50:269–288.[PubMed]
Freeman MP, et al. Omega-3 fatty acids: evidence basis for treatment and future research in psychiatry. J Clin Psychiatry. 2006;67:1954–1967. [PubMed]
Pifferi F, et al. (n-3) polyunsaturated fatty acid deficiency reduces the expression of both isoforms of the brain glucose transporter GLUT1 in rats. J Nutr. 2005;135:2241–2246. [PubMed]
Flachs P, et al. Polyunsaturated fatty acids of marine origin upregulate mitochondrial biogenesis and induce β-oxidation in white fat. Diabetologia. 2005;48:2365–2375.
Molteni R, Barnard JR, Ying Z, Roberts CK, Gomez-Pinilla F. A high-fat, refined sugar diet reduces hippocampal brain-derived neurotrophic factor, neuronal plasticity, and learning. Neuroscience. 2002;112:803–814. [PubMed]
Corrada M, Kawas C, Hallfrisch J, Muller D, Brookmeyer R. Reduced risk of Alzheimer’s disease with high folate intake: The Baltimore Longitudinal Study of Aging. Alzheimers Dement. 2005;1:A4.[PMC free article] [PubMed]
Fioravanti M, et al. Low folate levels in the cognitive decline of elderly patients and efficacy of folate as a treatment for improving memory deficits. Arch Gerontol Geriatr. 1997;26:1–13. [PubMed]
Nilsson K, Gustafson L, Hultberg B. Improvement of cognitive functions after cobalamin/folate supplementation in elderly patients with dementia and elevated plasma homocysteine. Int J Geriatr Psychiatry. 2001;16:609–614. [PubMed]
98. Ramos MI, et al. Low folate status is associated with impaired cognitive function and dementia in the Sacramento Area Latino Study on Aging. Am J Clin Nutr. 2005;82:1346–1352. [PubMed]
Fava M, et al. Folate, vitamin B12, and homocysteine in major depressive disorder. Am J Psychiatry. 1997;154:426–428. [PubMed]
Liu J. The effects and mechanisms of mitochondrial nutrient α-lipoic acid on improving age-associated mitochondrial and cognitive dysfunction: an overview. Neurochem Res. 2008;33:194–203.[PubMed]
Holmquist L, et al. Lipoic acid as a novel treatment for Alzheimer’s disease and related dementias. Pharmacol Ther. 2007;113:154–164. [PubMed]
Perkins AJ, et al. Association of antioxidants with memory in a multiethnic elderly sample using the Third National Health and Nutrition Examination Survey. Am J Epidemiol. 1999;150:37–44. [PubMed]
In this article, Team LoCoFit Coach Gillian Sanfilippo discusses the importance of an offseason, and the best way to execute one to set you up for a successful fat loss phase. If you are interested in coaching, where we apply these principles and methodologies to bring you to your best physique, click the button at the bottom of this page!
It’s no secret that Instagram followers like seeing lean physiques and stage shots (even more than food porn. I know, crazy). We’ve gotten to a point where you can never tell what is realistic anymore. So many competitors post throwback after throwback, but what about the present? Who are you when you’re not stage lean? Social media platforms are easily turned into highlight reels. You show people what gets the most likes, even if it portrays the wrong image.
The beautiful thing about bodybuilding is the fact that we get to build the physiques we want. There are seasons to grow and shape what we want to look like when we step on stage again. The time spent in the off season is just as much a part of this sport as getting shredded is. We all have a favorite, I’m sure, but you can’t have one without the other and expect to go far. I myself love having photos to look back on and I look at my stage shots as an accomplishment! It takes some serious work to get stage lean and having those photos will always motivate us. Nonetheless, we need to remember there are two important seasons we take part in as bodybuilders. One of them doesn’t happen to get as much spotlight as the other.
A trend that I’ve seen more and more recently is treating the off season as some kind of ‘how-much-can-I-eat-and-stay-lean’ challenge. Some kind of competition to show off all the food you’re eating at your body composition. That itself is contradictory to the main point here. You don’t just get shredded and try to stay that way, nor should you expect that when you dive into competitive bodybuilding. The off season is honestly where you’ll spend a majority of your time. Why? Because it’s real life and it’s the most sustainable place to be both mentally and physically.
My main point is that you need to take time to grow and should fully expect that when you’re not preparing to step on stage. An off season cannot be spent only a couple of pounds over your stage weight. Physiologically, it is not realistic or healthy in the long term. There are so many factors to consider including but not limited to hormones, blood panels, hair/nail health, training recovery, and rest. Who ever seems to be walking around shredded year round are either fooling you or failing to see the importance of taking time off. If you want to go far in this sport, you need to take the necessary amount of time to recover from the diet, grow, and get back to a healthy baseline. Both of these phases should be embraced in the sport.
Now that’s not to say we need to go into a full on bulk (been there, done that). We can easily go too far either way. Putting on unnecessary body fat will not only make us feel ‘bleh,’ but it won’t help us in the long run. It just gives us more work to do (aka more weight to lose) next time you enter a dieting phase. Most of the time, traditional bulks just end in more body fat than actual muscle gain.
As both a competitor and coach, I think it is incredibly important to be prepared. Competitors should be fully aware of what to expect when dieting for a show as well as what to expect in the months afterwards. Having realistic expectations is going to make the transition from prep to off season much easier on you. Keep in mind that you’re an athlete based on your discipline and work ethic. The hard work you put in will show even more when you get on stage and beat your last physique!
The information contained in this website is not intended to recommend the self management of health problems or wellness. It is not intended to endorse or recommend any particular type of medical treatment. Should any reader have any health care related questions, promptly call or consult your physician or healthcare provider. No information contained in this website should be used by any reader to disregard medical and/or health related advice or provide a basis to delay consultation with a physician or a qualified healthcare provider
We’ve all heard of the importance of mindset for creating the life you want, reaching your goals and the like. And everyone knows how powerful the placebo effect is in our lives. [Side note, don’t know much about placebo effect but are interested in learning more? Check out this amazing book Suggestible You] But did you know that your mindset can even influence your satiety?
In a study done at Yale in 2011, researchers studied the effects of the hormone ghrelin in response to either an ‘indulgent’ or ‘sensible’ shake. First, what is ghrelin? In the words of the researchers, “Ghrelin is an essential indicator of energy insufficiency. When energy intake is low or the stomach is empty, ghrelin is secreted from the endocrine cells of the stomach and transported in the bloodstream to the brain, where it binds with receptors in the arcuate nucleus and the ventromedial hypothalamus to produce the sensation of hunger and motivate consumption. As energy intake increases and nutrients are detected in the gastrointestinal tract, ghrelin levels are suppressed, thereby signaling to the brain via neural and endocrine mechanisms to reduce appetite and increase feelings of satiety.” In layman’s terms, ghrelin is a gut peptide that regulates our appetite.
Traditionally appetite regulation has only been looked at through the lens of calories. A higher calorie, more satiating meal will increase ghrelin while the opposite will happen with a lower calorie meal. While this makes logical sense, it’s not that straightforward.
Subjects were given two shakes at two different time points. One shake was touted as a high calorie, “indulgent” shake. The other was touted as a low calorie, “sensible” shake. In reality, both shakes were exactly the same. Ghrelin was intravenously measured before, and after ingestion of the shake at two time points. Specifically, 20 (pre shake), 60 (post shake) and 90 minutes (post shake).
The results were pretty astounding. Subjects had a steeper rise in ghrelin during the anticipatory period before the indulgent shake followed by a significantly steeper decline in ghrelin post drinking the shake. However, “when drinking the shake in a sensible mindset, participants exhibited flat or slightly increased levels of ghrelin over the course of consumption suggesting that, despite consuming the same nutrient contents, they were not physiologically satisfied.”
As a coach and a physique athlete, this research is incredibly important for me to understand. Simply how we view our food can determine levels of satiety, effect cravings and potentially derail progress. Since we are bombarded daily with both “indulgent” and “healthy” labels, this is important for consumers (all of us!) to understand.
If you’re interested in the full text and want to get your nerd on, click here to read. Thank you for reading! We hope you find this informative and helpful!
Laurin Conlin, Founder and Coach at Team LoCoFit
All information, content, and material of Team LoCoFit is for informational purposes only and are not intended to serve as a substitute for the consultation, diagnosis, and/or medical treatment of a qualified physician or healthcare provider.
Sleep is one of the most important factors for maintaining our health and not becoming another statistic of heart disease, diabetes, or any of the other common ailments most 20th century Americans have grown to accept. It’s also how we repair our body and mind and adapt to a training stimulus to get jacked and lean.
How we go about battling our environment for our survival and health is a multi-faceted question with many possible deficits and potential solutions. We must dig a little deeper and look into the seemingly unrelated aspects of life both inside and outside of our bodies.
When sleep is poor and or “perceived” negative stress is high, we begin to read our very own “bad” genes. “DNA is simply a blue print it’s either on nor off, it is either read, or not read” (1). When we perceive the stressors in our lives as bad instead of potential learning experiences to help us become better, we start to trigger a cascade of stress hormones. If our sleep is high quality sleep and we experience all the phases including light, REM and deep sleep, the body and mind heal themselves. That’s right they heal themselves.
Second, have a positive attitude and welcome the stress. Greet it with a warm smile and say bring it on! Make me better! As my old high school wrestling coach would say “Iron sharpens iron.” With no adversity, we cannot grow. The conscious and subconscious mind must be on board and practices like meditation, hypnotism, repetition and other tools known as energy psychology such as “Psych-K, Emotional Freedom Technique (EFT), Theta Healing, Holosync” can help you get your subconscious mind fully on board. This must be a priority as the subconscious mind is on 24/7 and the conscious mind is only active when we are purposefully thinking about something. (1)
If you’ve heard me speak before I almost always touch on the topic of sympathetic vs parasympathetic state. Both states can have a profound impact on our physiology, health and performance. We need to be able to scale in and out of each as needed and not wind up being trapped in one of them. Mainly we speak about being too sympathetic aka too much fight, too much adrenaline, too much cortisol release, too much restlessness and not enough rest, sex and digest ( parasympathetic). This is paramount when it comes to sleep. If we are always in our defensive mode, then our bodies are “prepared” for the “next attack” which could come from the monthly bills, the boss, traffic, or even missing our next meal. Our mind and body are treating each of these perceived threats as a real threat to our survival right here and now. Now we can’t sleep well and it becomes a snowball effect of bad days and nights which stress you out even more. We must CALM DOWN!!! Woosah, as I like to say (Bad Boys II). Use your ability to change your perception and be more mindful of your thoughts. A positive state of mind can help any situation. A bad state of mind can hurt any situation, even a seemingly good one.
Physically improving sleep is the next step in our two pronged attack on improving quality of life and performance. We have a few tools, supplements and lifestyle factors to play with here. If you suffer from sleep apnea the number one quick fix is purchase a CPAP. If you snore, momentarily stop breathing (sleep apnea), kick your leg a ton (restless leg syndrome) or just generally feel groggy and never experience a refreshed feeling after a full night’s sleep, then ideally we would like you to get a sleep study before purchasing a CPAP to see what the exact cause is for why you’re not sleeping well. If you’re positive you suffer from sleep apnea then purchasing an “autoset” CPAP out of pocket will get a jump start on improving how you feel immediately. I personally use a nasal pillow mask (nasal breathing has benefits over mouth breathing we will discuss at another time). If your sleep study shows you are experiencing apnea, buy a CPAP out of pocket or through your insurance. Bam!
If you are not getting into REM and deep sleep, but don’t suffer from sleep apnea, we can look at blood labs (if apneic still do this as well). Specifically, we will use Dr. Stasha Gominak’s 10 years of experience through the patients at her practice and the reference ranges she has provided for us. She has found that our modern lifestyles (indoor AC and limited sunlight) have allowed our “bad” genes to sky rocket since the 1970 . Why is this so? We have a vital hormone that is only produced via our skin receiving UVB light from the sun. This hormone is D3. Otherwise wrongfully name vitamin D3. It is a hormone and an extremely powerful one. We need our D3 ranges to be 60-80 ng/mL optimally. The normal range is 30-100 ng/mL but this is too large of a range. Too low or too high and you will experience negative side effects including disruption of mood, sleep and physical pain. (2)
If vitamin D3 is low enough for long enough, it then affects the gut microbiome and vitamin B’s status. Dr. Gominak pays particular attention to vitamin B12 and B5 specifically. She says B12 needs to be over 500 pg/ml to experience normal sleep. The normal low range number is 225 which is too low in her experience. B12 can be easily tested through labs however B5 has some issues with testing due to the way the body stores and reserves from what I understand. Her recommendations are as follows. First, supplement all of the above until D3 is in range. That means to begin supplementing with D3, B12 and B50 or B100. Sleep should improve but may take months or years to heal, depending on the extent of prior damage. Most healthy readers should not take this long. Then, as soon as sleep begins to deteriorate, you begin having muscle aches and pain, or you are irritable and cannot sleep, drop the B50 immediately and within 1-2 days the side effects will cease. You have now allowed your microbiome to produce its own correct intestinal bacteria and supplementing B 50 or B100 is no longer needed. As D3 increases up to a healthy range, our sleep becomes deeper and our ability to heal increases meaning the B vitamins must be up and ready at bat. If you’ve been supplementing with D3 for awhile without also supplementing with B vitamins, this can cause additional problems including “pain and stiffness in the morning”. The two generally need to be supplemented together for optimal health. (2)
Night time routines and habits are the icing on the cake once the mind and body are right. We have some tricks and tips that I have used for years now being a fireman with a wonky schedule.
Try and get off your phone and electronics 2 hours prior to bed. I know this is a challenge for all of us especially those that are hard workers and want to take extra advantage of every hour provided during our day. I get it. But ideally this allows the mind to settle down and physiologically allows the body to begin producing melatonin when light is dim and it slowly becomes darker and cooler. This signals our body that it is time to start preparing for a deep sleep. Plus read a damn book.
If you have no option and must be on your tech devices at night turn the brightness down and place them on night mode if you have that option. This technology is still up for debate as for if it works effectively or not as the screen is still emitting blue light. But it’s better than nothing. If you have lights in the house with dimmers utilize them and or red light bulbs. If you want to be really cool like me you can wear blue light blocking safety glasses which block basically all visible blue light. Blue is the easiest color for our eyes to detect in the visible spectrum so it is of vital importance that we lower the amount our eyes receive at night.
Supplementing melatonin if you do not have a regular sleep-wake cycle can help you go to sleep and reset you clock hormones. Melatonin should be taken 1-2 hours prior to bed the closer to bedtime the smaller the dose taken as to not allow the timed release to peak too late at night and cause drowsiness upon waking. Dr. Parsley recommends .3 to .5 MG but I have personally done 3 MG right before bed and not noted any problems. I also sleep for 7-10 hours depending on the day so that’s my N=1 study. (3)
I hope these tips and tricks I’ve learned over the years provide you with more than enough resources to begin experimenting with yourself to help optimize your sleep. The resources I have learned from I highly recommend and encourage you to seek out more knowledge from them.
Dr. Lipton Interview- https://www.youtube.com/watch?v=GCG1zj3mxOw&t=2261s
Dr. Lipton Subconscious Mind- https://upliftconnect.com/reprogram-subconscious-mind/
Dr. Gominak interview- https://www.youtube.com/watch?v=74F22bjBmqE&t=185s
Dr. Gominak and Vitamin D Supplementation- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5541280/
Dr. Gominak Healthy Gut Bacteria- https://drgominak.com/2017/12/16/healthy-bacteria-healthy-sleep/
Dr. Parsley Interview- https://www.youtube.com/watch?v=Akw0zGlaIT4
Blue Light Harvard Study- https://www.health.harvard.edu/staying-healthy/blue-light-has-a-dark-side
Written By: TeamLoCoFit Training Director Ryan Conley
Physiological processes are constantly occurring within our bodies in an effort to maintain homeostasis. The fact that we have such a complex nervous system which allows us to make incredibly smart decisions and self-regulate is one that sets mammals apart from most other creatures on earth. (2) When our bodies interpret a situation as stressful or threatening, mechanisms are utilized and adaptations occur in an attempt to reverse the threatening situation and get back to a state the feels “safe”, aka restore homeostasis. One of these adaptations which gets examined frequently in the health space, particularly in the context of weight loss or getting to extreme body compositions such as in the sport of bodybuilding, is the decrease of the hormone leptin throughout a period of caloric restriction.
What exactly is leptin?
Leptin is a protein that is primarily synthesized by white adipose tissue. Leptin has strong ties to energy stores, is crucial in determining satiety, and appropriate levels are required for proper meal termination. Without a sufficient level of leptin, an individual will have trouble feeling full or “satisfied” after a meal or in between meals. (3,4) Leptin travels through the bloodstream and acts in the satiety center of the brain, (a subregion of the hypothalamus called the ventromedial hypothalamic nucleus) the VMN, to keep appetite and adiposity in check. Typically, the more fat tissue a person carries, the higher his/her level of the hormone, and the less fat tissue a person carries, the lower his/her level of the hormone.
Research on leptin such as the study done by Trexler et. al, (2014) state that short-term energy restriction and lower body fat levels are associated with decreases in leptin. In the context of bodybuilding, a case study carried out by Rossow et. al, (2015), found that leptin levels were nearly cut in half from the beginning of the competition diet (2.58ng/mL) to 6 months later at the time of the competition (1.36ng/mL). Clearly, leptin aids in the regulation of energy homeostasis, so it is no wonder that this hormone is disrupted when homeostasis is diminished through a period of caloric restriction. (1)
How exactly does leptin act?
Leptin operates in a similar way to the thermostat in your home. There is a feedback system between the VMN and leptin that will elicit increases or decreases in the hormone depending on the current state of your body composition in relation to what your body “wants” your composition to be (think your set point). As your body fat levels start to decrease, so will your leptin levels. As this is happening, you may notice your appetite beginning to ramp up making it harder for you to maintain the deficit – which is just what your body wants to happen. (2) You may also start to experience extreme food focus or food anxiety because your body is begging to be fed. The ideal situation from a homeostasis perspective is that you will begin to satisfy the feeling of hunger by eating food until you have returned back to a range around your set point. Essentially, low leptin levels elicit a profound starvation response. (2) Research has also shown other inevitable adverse adaptations that occur during a period of caloric restriction such as decreased metabolic rate (you will have to eat less and exercise more to lose weight further), decreased non-exercise activity thermogenesis (you will not fidget as much, etc. in an effort to conserve energy), activation of brain reward center (you will become hyper-focused on calorie-dense foods), and increased levels of ghrelin (the hunger hormone.. stay tuned for more on that).
How can we combat these adverse effects of dieting, particularly the decrease of the hormone leptin? While these adaptations cannot be avoided while dieting, there are protocols that can be put into place over the course of a diet to help attenuate them.
Do not diet too harsh for too long. The longer you are in a deficit (regardless of severity), the more set up you are becoming to regain body fat. Research has shown that even a short-term caloric restriction will begin to reduce levels of leptin, so don’t overstay your welcome in this phase.
Incorporate diet breaks. Give yourself long enough to diet that you can take the occasional diet break (1-2 weeks of eating higher calories) to give your body a bit of a break and take it out of the stressed-out state.
Eat higher protein for the satiety effects
Do not diet too extreme right out of the gate. You should always start at the minimal effective dose: what is the most you can eat, and the least amount of expenditure needed to move the needle.
Resistance training may help keep the lipostat satisfied. The hypothalamus is the body’s lipostat which is the brain region that regulates appetite and body fatness. As you lose fat, the lipostat will engage the above-listed mechanisms to try to promote regaining the lost fat. (2)
While we may not be able to inhibit the mechanisms put in place by our bodies to maintain homeostasis (which we should be grateful for), being aware of the adaptations and making the most educated moves possible to respect our bodies while working towards a goal is imperative and can make the process much smoother.
Bouret, S. G., Draper, S. J., & Simerly, R. B. (2004). Trophic Action of Leptin on Hypothalamic Neurons That Regulate Feeding. Science, 304, 108-110.
Guyenet, S. J., & Aoki, S. N. (2017). The hungry brain: Outsmarting the Instincts that make us overeat. New York: Flatiron Books.
Keim, N. L., Stern, J. S., & Havel, P. J. (1998). Relation between circulating leptin levels and appetite during a prolonged energy deficit in women. American Society for Clinical Nutrition, 68, 794-801.
Morton, G. J., Blevins, J. E., Williams, D. L., Niswender, K. D., Gelling, R. W., Rhodes, C.J., Schwartz, M. W. (2005). Leptin action in the forebrain regulates the hindbrain response to satiety signals. The Journal of Clinical Investigation, 115(3), 703-710.
Rossow, L. M., Fukuda, D. H., Fahe, C. A., Loenneke, J. P., & Stout, J. R. (2013). Natural Bodybuilding Competition Preparation and Recovery: A 12-Month Case Study. Sports Physiology and Performance, 582-592.
Trexler, E., Smith-Ryan, A., & Norton, L. (2014, February 27). Metabolic adaptation to weight loss: implications for the athlete. Journal of the International Society of Sports Nutrition, 11, 1-7. DOI:10.1186/1550-2783-11-7