“If you eat and drink more calories than you burn off, then you’ll gain weight,”–Coca-Cola
Coca-Cola would have us believe that by not controlling our calorie intake, and therefore our weight, we are the cause of our own obesity. However, if obesity is instead created by an imbalance in our ability to regulate stress, where stress regulates calorie desire, storage and expenditure. This is would be why the quality of the calorie is more important than the quantity of calories.
Metabolic disorders created by too much stress occur for multiple reasons. Sugar and fat are natural sources of energy. Within the context of the whole foods or the whole meal buffer the “tax” we pay for that energy. We overeat these high fat-sugar-salt meals without whole foods which causes more stress, in which we then seek more resources. It becomes a vicious cycle.
Direct Causes are not Real Causes
Direct causes seem like they are ”the” cause or solution, but in reality the “molasses” they exists in really controls their nature and action.
Outcomes are caused more by the “molasses” or the stress mechanisms calories exists in. It is the stress that is the true cause, not the energy unit of a calorie itself. It’s very easy to get fooled into thinking the most obvious answer is the correct one, but often times it is a complex regulatory undercurrent that is really in control.
Putting the Calorie Model in its proper place
Calories in/calories out would make the situation very simple, but that is why linear logic can be so deceiving. It is an over-simplified attempt to account for the whole. In the short-term it can be true, but in the larger context it just doesn’t work. Calories are true but they are part of a much bigger story, which makes them false as a model and the wrong framework.
The conversations would therefore be better discussed in a “Complex Systems Model“. Obesity would now shift from a focus on the energy expenditure model to a focus on a communication and stress regulation model. How systems interact with stress, resources and adaptation. So instead of looking at eating right and exercising for calorie burning to balance a number, we’d look at eating right and exercising as ways to create better adaptations to environmental stress. Exercising isn’t about “burning” calories, although that happens, but rather engaging the system in physically challenging activities that engage the system to more fully utilize its energy resources and feel less prone to save them. Stress mechanisms inform the system about what type of challenges it is experiencing, what type of resources it has present and what it must do to try to regain balances.
Let’s explore the physics as to why calories are not central: A Manifold
See that small flat dot? That would represent calories. Calories are one of the flat parts to a circle, the round world of food and health. Calories are the most practical and direct cause; a flat-world cause of weight gain. The problems come when we start thinking the world is actually flat or when we continue using “Euclidean Space” dynamics of simple math to take on a complicated phenomenon as the human body and health, which needs non-Euclidean, round-world principals. The same problems occur if you take out one aspect of any complex ecosystem—you cause more problems.
Flat-world philosophies are an approach in science called linear science. Linear science finds single variables to find facts about the world. Another scientific approach is called nonlinear science and this science (which are rules used to discover truth) is about the interactions and complexity dynamics of the world. It’s by far a much more appropriate science to use, as it takes the linear information and puts it into real life complex scenarios. It’s not the absolute answer science of hard linear facts, but the softer fuzzier complex science that represents “what ifs” and “maybes” and “depends on the context”, aka “real life”.
Calories are a flat-word science.
The over-application of linear logic or the assumption that the use of nonlinear science wasn’t necessary or too complicated, led us to the assumption that flat science would work just fine. The problem is that the parts, the linear facts, don’t make, nor do they apply to the whole (without consideration of the whole). Flat lines, if you put them all together, will never create a curved line. You have to switch the science (the rules you use) and start looking at interactions. Linear science is what tricks people into thinking that we could just focus on calories, even when we had evidence there were larger things going on within the body that played bigger parts in this energy balance. That assumption of focus on the calorie as “good enough” trapped us into misleading logical confines called a “false dilemma” or a “false dichotomy”. It’s thinking that since we assumed calories are the cause we had only two choices to solve our problem: to eat less or exercise more.
“Logic is a systematic method of coming to the wrong conclusion with confidence” ~Murphy’s Law
The number of calories isn’t what causes obesity, what that number communicates is what causes obesity.
It’s a round world of complex interactions. A small but significant shift from thinking there are only so many calories we can use (burn), to thinking there are only so many calories we can manage (stress). Calories in/out or other single causes, however crucial, are only small flat parts of the much larger issues we must engage with to manage metabolic and noncommunicable disorders.
From Ignoring Evidence to Applying it
What are the prominent associations and causes of obesity?
- Genetics: Genetically susceptible populations
- Epigenetics: Genetics being altered, adapted and programmed by the environment
- Positive Energy Balance: Too much energy IN and not enough OUT. Fast foods and sedentary lifestyles.
- Microbiome: These little guys developed with us in a symbiotic relation: We give. They give. Without them, it makes things harder, more stressful with fewer resources and more susceptibilities.
- Pesticides and BPA: Endocrine disruptors alter our orchestrating hormones that tell us what to expect in the environment and how to respond accordingly.
- Sleep Disturbances: A two-way street, the more stressed the less we sleep, the less we sleep the more we are stressed.
- Vitamin D: Also a two-way relationship in obesity, suggested as a cushion for inflammation. However, Vitamin D from the sunis a much under-appreciated hormone that has a foundation in our development, immune functionality and integrated systems such as skin integrity and our microbiota. We were built with the sun as a resource, it would only make sense we would make use of it and need it.
In a linear paradigm, it’s about single causes, so many in science look at this list and say “Yes, but which ONE causes obesity?” When there are so many possible answers or different combinations that can potentially create an outcome, many of our instincts want to assume it’s too confusing, or none of them are correct and we dismiss them all. Thinking that behind the scenes “somewhere” we will find that single cause. However, in a nonlinear paradigm, because it’s about stress channels, any combination can bring about the outcome, so they can all potentially work to create the situation of metabolic distress and energy regulation issues. Stress is that single cause, but stress itself is never a single cause, it’s a system balance. So all of these aspects are necessary players when we look back at our history of evolving with interconnected partners that developed strategies to become resilient and grow from stress and become potential “causative factors”. When you shift paradigms the same evidence brings you to very different conclusions. The wrong scientific parameters, perspective and current environmental decisions based on the wrong paradigm are the true cause of obesity.
——–Putting it all together————
The scientific paradigm of Chaos dynamics is much like looking at weather patterns in particular climates. Weather patterns, or chaos, are about “sensitivity to initial conditions”. Meaning the outcomes are wholly dependent on where you start. While not predictable it is determined by specific sets of variables acting upon these variables. The thing acting upon the system does not alone create the outcome; the system interacting with the inputs is responsible for the outcome.
ESTROGEN COULD BE THOUGHT OF LIKE THE EAST COAST
Chaos: Initial conditions —-> Variable influences —-> Predictable but unpredictable outcomes
When applying a chaos physics model and thinking of our human health like weather patterns in particular climates, we first need to find our “initial conditions” or starting points. This is where influences create divergent outcomes. We could reduce our initial conditions to genes but that’s a little like reducing the tree to the tips of its roots. They’re informative and they matter but it gets easier if we find other “hubs” where the environment influences individuals within expected patterns. Hormones that impact brain development, sensory and information processing systems (stress perception) and are genetically driven could be one of those hubs.
Estrogen impacts brain development as well as grey matter and white matter in the brains of both men and women creating distinct patterns of development, unique patterns of stress reactivity and patterns of susceptibility to outcomes. We also know from researchers like Deborah Clegg that estrogen can be seen as an orchestrator of energy regulation and glucose homeostasis as it is a prominent channel that communicates stress and fat storage, immune reactivity, obesity, adiposity and energy dysregulation in the brain.
Hormone-driven functioning creates variety and diversity. Genes in cases like gene-environment interaction don’t program for diseases like we once thought, as in “it just runs in the family” and can’t be avoided. Rather genes program for particular function and typically better survival. We could think of it as these functions have particular fuel needs and operate within certain pathways that keep them regulated and balanced. When those particular resources are compromised the function and its needs create distinct thresholds and outcomes. Gene-hormone set-ups are not destiny that one will fall into a disease-state but rather those genes set up unique requirements that must be obtained and balanced or you find yourself in a stress-associated disease state.
Genes and predispositions are not your destiny to a disease, but rather a function that requires attention and respect for the coping mechanisms and resource it needs to thrive. The foods we eat, the stress we are under, turn genes on and off in response to those resources and challenges. Tweaks from the environment. Stress isn’t a thing; it’s an action, a model, so that action first and foremost depends on where one’s particular ‘bar’ is set and the thresholds we establish from early exposure. This correspondence to react to the environment is about building resiliency and raising the bar of stress resiliency by proper environmental conditions, like quality foods we evolved with.
Is Obesity a Math Problem or Communication Problem?
What happens when we move from speaking about obesity as a math problem to obesity as a communication problem is we find we may be getting the wrong directions and insufficient resources from our environment. Calories are still part of the equation because the body begins to seek and store calories (energy) when the body has more stress (challenges) and it needs more resources. This would make sense that our bodies and brains are highly adaptive to our environments. We need accurate information and communication about what is going on or we will falter. We build the wrong or unnecessarily strong structures or save resources with too many shortcuts. This is about communication.
Estrogen and its contrasting subreceptors, alpha and beta, communicate to the body/brain what is happening out in the environment and adjust accordingly. We have times or “critical periods” while in the womb, toddlers or teenagers where they are even more aware and pliable to change. This is partly why we see many studies on the impact of “endocrine disruptors” like pesticides, BPA or plastics in obesity. They interrupt or accentuate this communication. While in the womb a person can be “programmed” to overly store energy in preparation for a hostile or lack of tools and materials environment.
So we have particular hubs of divergent points that alter how the environment impacts us. You could think of this like a PLINKO! Board that has varied influences that lead to predictable but unpredictable outcomes. The important part to consider is that this is very different than our assumptions that single influences are to blame for each particular outcome.
That is the paradigm shift. You don’t look for evidence of one particular thing that effected everyone who is obese. There will not only be a wide variety of influences,and starting points, but also delays, adaptation and programming. It is not one-to-one and it’s not one direction of cause creating an effect (outcomes can double back and become part of the causation). So any exposure can reprogram the system creating improper reactions to the environment, which creates seemingly inappropriate seeking and storing. The oddest part is that this can even create improper reactions to what we think of as “healthy” foods. However, unlike the current paradigm, where we think if sugar is the problem and we take it out we should see it “fix” the problem. Rather, we may have to address the system, the context the sugar comes in, or we would need to look at “reprogramming” the system, not just the absence of the cause (sugar).
If some of us are getting messages from the environment about stress, like from estrogen disruptors (see NYTimes article “Warnings from a Flabby Mouse“) that do not represent the actual environment, this can create false messages of stress. Of course that is just a start, or sometimes a small stage setter of false messages of stress from the environment. Certainly our food supply is another stage-setter and susceptibility modifier for estrogen disruptors (lack of nutrients increase toxicity of pollutants). This creates greater susceptibility to those more highly genetically in-tune (estrogen receptivity variances as suggested by personality and anthropologist researchers such as Helen Fisher PhD) to this type of “stress” information. There are also plenty of real messages of stress that hit others of us and contribute to the problem. And beneath those platforms? Well that’s our foundation, our partners in evolution, our gut bacteria. This is where our immune system communicates and supervises the thousands of switches that attempt to help us balance stress.
Another communicator within our stress, organ and immune systems are our synergistic partners within our microbiome. We’ve developed this relationship over centuries both by eating them directly in our fermented foods, developing communication with them and by feeding them with our complex diets from within our diverse cultures. They are an important aspect of human nutrition and stress balancing. Probiotics, our fermented foods (dairy, grains, vegetables, fruit) dating back 10,000 years (Princeton) and prebiotics, the fiber and sugar our little gut microbes rely on. And as authors Kau describe in their June 2011 article in the journal Nature, our current “dramatic changes in socioeconomic status, cultural traditions, population growth, and agriculture are affecting diets worldwide” and our little synergistic friends, our microbiome.
Cecil Lewis anthropologist discusses that our microbiota have changed dramatically in the last 100 years. There is also evidence from Professor Cooper and researchers at University of Adelaide’s Centre for Ancient DNA that there have been changes even in the microbiome of our mouths in these last 100 years. Our rural -cousins resemble our ancestors more than city-dweller and maintaining this relationship and diversity appears of the utmost importance, especially to our ability to handle, detect and respond to our environment, foods, and stressors.
Foods Help Regulate Stress
Foods are clearly a pivotal resource in recovery and resiliency to stress. However, the act of eating foods can also create a stress. A stress in the system here is a demand for attention and energy for an action. It takes energy to break down and make use of the foods we eat. Clearly 10-25% of our calories can go toward this digestion. There is a also stress to be handled with byproducts and processing we have to balance these loads. Foods that create stress for us aren’t inherently “bad” for us, but they can become so, by activating stress defense system when they do not have counterbalances and buffers. A steak is great for you, but it can create byproducts, drinking a glass of wine with your streak can buffer those byproducts making the meal less stressful. Stressful foods are many times foods where we get our best calorie resources like sugar and fat. Calorie dense foods are resources for other stresses from our environment; emotional, intellectual or physical challenges. Also maintained by these resources are our very expensive internal organs like the brain, heart, skin, immune, reproduction and so forth. Although various stressors like physical or emotional pain have unique pathways they also run many of the same pathways and feed from the same pool of resources. A true sensing and sharing organism. Nothing like the paradigm of separation of body systems and the separation of mind and body. This is a very bidirectional relationship and intimately integrated network of a very “intelligent” system even on the cellular level. The mind, sensing and awareness, is the body and vice versa.
Nutrition is often thought of as “filling up a tank”. In our current paradigm nutrition’s impact on health was thought of as either deficiency or excess, a very straight-line of “enough” or “too much”, a linear concept. What this neglects is that our body is a sensing system and that sensing system, call it the brain, immune system, stress regulation or gene expression is a powerful force in determining the trajectory of our health and growth from food. This is also more significant than “helping us grow”. It is more than a fuel needed in an already planned out system. Nutrition from our foods are in essence information about the environment we are entering and a constant interaction guiding us. So in a very subtle way it is not only helping us to grow, but rather directing us how, where, when and why to grow. We see this in the power of milk in the early stages of life. Another example is from the research and pivotal discoveries of Timothy Noakes. Our muscles are not like a physical machine that just needs gas to work. They don’t just have a fuel they run out of, but rather there is a complex communication within the nervous system and the brain that allows that energy to be dispersed and utilized correctly so we stay in balance. The physical aspects of “filling up a tank” may seem reasonable, but it is ultimately again an illusion that it is that hard and fast of a situation. It’s the undercurrents; the “ghosts” behind the workings that we rarely see and can often neglect that are true drivers of outcomes.
Our Internal Dance of Balances and Communication
Keeping what is called “homeostatic” balances of all the organs and activities of the body can be very delicate and sensitive. In a manner of speaking foods talk to us and give us an expectation of nutrients through sensory mechanisms and communication channels and the interactions between physiological processes. In this way our systems can sense what type of resources, like fat or sugar are coming its way. Foods really are more than just ‘fuel’ as they are actively communicating with the stress regulatory hubs like the mTOR system or the Hypothalamic-pituitary-adrenal ( HPA) axis) and the sensory system that is our brain.
Seeking True Needs and being Deceived
We seek caloric density because the body thinks is undergoing a time that its needs have greatly increased or been compromised because of threats. (This lately seems like always does it not?) So these calorie sources have multiple actions and signals. They are of crucial importance that we are motivated and learn where to get them. This is unfortunately what food manufacturers and chemist take advantage of, “mimicking” these powerful sources and supplying them to us cheaply and out-of-context. The sugar-fat-salt combination what is termed “palatable” meals or “junk foods” that taste (and feel) really good are taking advantage of, these communication pathways attempting to guide us and motivate us to get these resources and in these combinations. It is these combinations, in the natural form of a culinary feast that are high in this fat-sugar combination of caloric dense resources, but within the context of a meal the impact this has on the neuroendocrine systems is buffered by the other foods within the meal; the fruits, vegetables, fibers, quality fats, herbs and spices. Buffers found in natural foods eaten in context of traditional recipes and meals. However, the junk food as palatable high fat and high sugar foods with merely flavorings meant to imitate these meals and hit the right brain pathways for motivation and desire, stress us, and alters our balances and lead us on wild goose chases. Empty calories as processed foods are serious deceptions.
Sensing creates vulnerabilities: Taking this “sensing system” perspective to obesity would bring to the discussion these other factors such as endocrine disruptors, pollutants, early life stress, prenatal programming, community, family, microbiota, sunlight, naturalized environments, socializing, epigenetics and the impact these factors have on internal stress balances. This is a perspective why tweaking macronutrient balances like low-carbohydrate or reduced calorie diets create change not by solely reducing calories but by reducing stress or inducing adaptive stress alterations.
BUILDING A HOUSE: Why Real Food Matters
To better visualize the role calories, hormones, microbiota and whole foods play in this complex building of our bodies, we could think of it like building a house. Calories would be like the Men, the energy, to build the house. Our hormones are much like the Supervisors giving instructions and guidance. The Tools are the levelers, balancers, screws, hammers and the precision tools to put all the Materials to proper use. The Tools are the variety of phytochemicals we get with our fruits, vegetables, fiber, herbs and spices. The Raw Materials are what we get from meat, legumes, nuts, milk, fats and sunlight. Our Tools make sure our Materials are fully utilized (some Materials have built-in Tools and vice versa). Supervisors carefully follow our Blueprints, our genetic code from the thousands of years of experience and our epigenome, sort of like “scouts” trying to give us more immediate conditions and future projections. The Supervisors must also have a constant understanding of our Foundation; the land the house is being built upon. The Supervisors also survey the Climate to prepare for inclement weather and the Community for the services available if disasters should strike.
Elements of the Build
- Men: Calories: Energy from Sugar (and fat)
- Tools: Antioxidants, Inflammatory and Feedback balancers: Fruits, Veggies, Fiber, Herbs, Mints & Spices, Probiotics and Sunlight
- Raw Materials: Protein, Fiber, and Fats (Fatty Acids)
- Supervisors: Hormones, Immune System and inflammatory pathways; Estrogen, Gerlin, Insulin, Leptin, Oxytocin, Sirtuins, Orexin, mTOR pathways (to name a few)
- Blueprints and Foundation: Genetics, Epigenetics and adaptation to environmental challenges and the microbiome
In order to build a house we need solid blueprints, exceptional supervisors, proper tools, plenty of raw materials and of course just the right amount of strong capable men to get the job done. The number of men we need will shift depending on the other variables and stage of the build. However, if the blueprints, supervisors or feedback mechanisms aren’t on point, or if we’ve gotten false information from our surveyors, then the house itself, after being built, will need constant maintenance and will most likely start breaking down. It will cost us a lot of time and money. We can save money in the short-term and along the way of course by getting rid of our most obvious money drain, our labor costs. This may make it appear that the money problem was solved and therefore the men were the cause. However, calorie restriction as a solution to a problem doesn’t automatically mean that calories were the problem to begin with. There could be times lowering calories or firing men was successful because there were insufficient tools or materials for those men to use. Firing a dozen men off the job because you didn’t have enough tools for them doesn’t mean that the men were the problem. Calorie Restriction in many ways could be seen as the old paradigm approach of finding the “quick fix” to a problem without addressing the whole. Dietary Restriction makes adjustments in the behavior of the system to stress, but really it is the stress, why we are under and impacted by so much stress to begin with, why we lack the tools, materials and proper directions, that should be addressed. The least amount of calories you have (men showing up to do a job) does not build the best house. You need all the men you can get in balance with the most tools, materials, good supervisors and solid blueprints to build the most efficient, powerful and effective house you can construct. Reducing calories in that framework without the other considerations makes no sense, it only creates weaker houses.
So building a healthy body and maintaining a healthy weight is about a sophisticated communication and cooperation of an ecosystem of events and players that go into creating a well-functioning, highly evolved, elaborate system. Therefore getting calories in the context of whole foods, a whole meal with family, friends, and community seems the best and most imperative framework for understanding health.
Food isn’t a Magical Fix but an Evolutionary Foundation
“In other words, while the evolutionary causes of the enlarging human brain themselves are thought to have been due to factors that go beyond diet alone (increasing social organization being prime among the proposed factors usually cited), a diet of sufficient quality would nevertheless have been an important prerequisite. That is, diet would have been an important hurdle–or limiting factor–to surmount in providing the necessary physiological basis for brain enlargement to occur within the context of whatever those other primary selective pressures might have been’ Tom Billings @beyondveg.com
Food doesn’t magically fix us. We built a house of cards slowly as we found, combined, cooked, fermented and created meals with our food. Our bodies slowly figured out how to get and make better use of foods and find buffers for the foods we ate by following our tastes and driven by flavor. When we didn’t cook our food we couldn’t get enough calories from raw foods. When we didn’t have our gut bacteria it was difficult to get enough nutrition, so the microbiota ended up doing some of that work for us. As this greater supply of nutrition became available our brains grew in capacity and function, because we came to depend on that nutrition that built it. Our brains and bodies are marvels at compensating and adapting and figuring out ways to save energy and find nutrition, but sooner or later the body can only compensate so much, so far. It becomes overprotective, over-seeking, and overly needy and must become stingy on where it sends its energy and how it’s going to save it.
“Thoughtful leaders increasingly recognize that we are not only failing to solve the persistent problems we face, but are in fact causing them.” John Sterman, 2002 MIT speech “All Models are Wrong: Reflections on Becoming a Systems Scientist”
Fats are fattening, germs are bad, and the sun causes cancer. The logic of “if it’s bad get rid of it” may actually have caused more problems than it attempted to solve. Fats, Germs (our gut microbiome) and the Sun (nutrient hormones produced from sunlight) all make a difference in our immune systems, neuroprotection and stress regulation. These factors impact our energy regulation (fat storage), adaptive mechanisms and our behavior. Without the protectors we evolved with, the stress of every day life and exposures can become more stressful. Without resources this alters when our bodies perceive threats and subsequently begin over-reacting to our environment. We essentially have lowered the bar in our ability to handle stress. Our bodies end up finding ways to protect and compensate from these stressors and this typically ends up expressed as various disorders, protective strategies and trade-offs.
“We can’t solve problems by using the same kind of thinking we used when we created them.” – Albert Einstein
What causes stress in Obesity?
- Calories. Too many calories don’t just fill an arbitrary tank. That tank being over-filled causes stress. Imagine 100 men show up to do a job on a house and you only have tools for 50.
- Sugar. Sugars are a primary energy source. Too much sugar, especially in refined form, especially in forms reduced, cheapened and further isolated forms, like table sugar or High-Fructose Corn Syrup cause stress. Sugar needs to be in balance, like the men, with the tools, materials and natural buffers. Energy from carbs requires a tax to be paid from the byproducts and breakdown.
- Fat. Too much fat without balance. Too much fat of the easy cheap variety creates all sorts of problems. The introduction of manufactured vegetable oil fats that came into existence in the early and late 1900’s and proliferated in the 1970-90’s , because of an oversimplified and over-applied assumption about fats. Fats in this reduced stripped down form causes stress on the system. Fats need to be in balance with the tools, materials and other fats in to buffer and balance the stress and inflammatory balances of the system.
- Not enough Fat. Getting rid of natural fats from animal products like dairy. The saturated and natural trans-fats, and the multitude of other nutrients and combination of fatty acids buffered the stress on our systems. Omega-3 fats especially disappearing from grass-fed animals in the combination and balance we evolved with were part of how our bodies and brains built and protected itself. Their absence causes us stress.
- Germs. Getting rid of germs. Not just antibiotics, but when it comes to foods, the naturally fermented products from unpasteurized dairy, fruits (aka wine), fermented grains like alcoholic beverages with their diverse social and cultural history (which also requires caution), vegetables and naturally cured meats. These products assisted and developed our microbiome, the germs that reside in our guts for thousands of years depend and our built because of what we ingested. These germs of our guts help us digest food, produce vitamins for us and regulate our genetic and immune expression. Without this diversity our environment causes us more stress.
- Processed foods. Refining foods causes us a multitude of issues because it throws off our balances. The context of the meal, the foods that we combined and fashioned into delicious recipes that provided us with a rich balance of interactive constituents. Processed foods could conceivably make nutritious foods more stressful to us.
- Pesticides and Pollutants. Another reason to re-examine our corporate “big” farming practices and environmental clean-up concerns. Endocrine disruptors in the environment do more than interrupt reproduction, they have the potential to make stress more stressful because they can, for example, impact endocrine signally for the brain and immune development. The growing climate change with increased Carbon Dioxide (CO2) in the atmosphere may be a contributing factor in lowering our ability to handle stress.
- Psychological Stress. A complicated sometimes primary other times more secondary player in stress obesity dynamics. Since many of these factors interact, enhance, diminish, or otherwise confound each other, the psychology will cross-over to the physical and vice versa via the multitudes of “cross-talk” among the body’s organs, stress perceiving and resource allocation hubs. Nutrition or other programmed immune interactions can set the stage to make stress more stressful and lower the bar for psychological or physical stressors to exert more impact.
- Epigenetic Programming. Information about the hostility of the environment from previous generations, parents and grandparents. Stress mechanisms start with initial conditions and those initial conditions can be altered to adjust to a “hostile” environment and modify their stress reactions and seek more resources.
- Our Approaches. When we blame an outside “thing” instead of the sensing system, we end getting rid of a stress instead of working with the system to be more reslient to stress. That stress-producing item may have been very valuable to us. Sunshine, for example, directly has the potential to cause skin cancer. Do we get rid of sunshine or do we need to address ways in which the sunshine may have become more stressful because of our nutritional choices, immune, emotional stress levels and the ‘sensing’ organ of the skin? Was blocking out the sun the answer? Or did that scientific paradigm logic of getting rid of things we need simply cause more problems?
A stress perspective is different than a cause-effect perspective. Cause-effect finds a cause and gets rid of it. Stress looks at balances and interactions. Calories are hard, linear and static model of what causes obesity. Whereas stress is a dynamic, interacting and nonlinear concept of what causes obesity.
Read More about how sauces with our meals help regulate stress —–> Does Daphne Oz Owe Bearnaise Sauce an Apology?
Simple steps to solutions:
- AVOID: Fake flavors, processed foods, trans-fats, msg, and high fructose corn syrup as they impede health and potentially the health of real foods by distrubing the ecosystem balances of our bodies and brains.
- Aware of individual needs and how foods impact stress regulation and the body as “sensing” systems
- Light whole foods and days mixed with heavy meals from time to time
- Grass-Fed and Whole animal eating; encouraging a larger variety than “lean meats”
- Fermented and cultured meat, cheese, vegetables, and dairy
- Fruits, vegetables, herbs and spices, nuts, grains as tolerated, real cheese, well-kept animals, oils-butter-lard (in moderation or oscillations), wine, beer and spirits naturally fermented and prepared, traditional and culinary-style simple eating.
- Exercise, fun, family, games, creativity, community, individuality
- Weight-loss; low-calorie, fasts, alternate-day fasts, surgery, low-carbohydrate or other health-reattainment type diets or lifestyles diets have a place in a stress model perspective
- A new scientific approach, an ecosystem and diverse approach, to health and well-being.
Moving to a new paradigm represents a framework that better suits and makes sense of the evidence. So besides changing our scientific framework from a single-cause, we begin using complex dynamics in stress-models. Solutions will be comprised of asking new questions. In my view it’s utilizing great diet programs already out there but generally what I like to think of as a “Culinary Lifestyle Diet”. Looking toward simply prepared foods from healthy animals with traditionally made sauces. Eating lightly most days, and feasts from time-to-time. Real foods including the miraculous ways recipes come together including fats, sugars and whole foods. Exercise, movement, challenges and games through sports and fun activities. Embrace and value the benefits of social connections with family, community, activities or friends. Clean up the environment; demand more from food providers and restaurants. Government to lift bans on real foods (from fear of “germs”) and to subsidize fruits, vegetables and small farms instead of the commodity crops. Embrace and take on stress, challenge our intellect, honor traditions, work to live don’t live to work. Schools incorporate diversity, creative learning, how to think instead of what to think. Our medical establishments to paradigm shift and include in their expectations an ecosystem nonlinear approach to health and recovery programs.
References for Causes of Obesity (2013):
For Full Reference List click HERE
- Genome-wide SNP and CNV analysis identifies common and low-frequency variants associated with severe early-onset obesity. Wheeler E, Huang N, Bochukova EG, Keogh JM, Lindsay S, Garg S, Henning E, Blackburn H, Loos RJ, Wareham NJ, O’Rahilly S, Hurles ME, Barroso I, Farooqi IS. Nat Genet. 2013 Apr 7. doi: 10.1038/ng.2607 LINK
- From obesity genetics to the future of personalized obesity therapy. El-Sayed Moustafa JS, Froguel P. Nat Rev Endocrinol. 2013 Mar 26. doi: 10.1038/nrendo.2013.57. LINK
- The genetics of childhood obesity and interaction with dietary macronutrients. Garver WS, Newman SB, Gonzales-Pacheco DM, Castillo JJ, Jelinek D, Heidenreich RA, Orlando RA. Genes Nutr. 2013 Mar 8. LINK
- What Mice Can Tell Us About Obesity by Alexandra Sifferlin January 9. 2013 http://healthland.time.com/2013/01/09/what-mice-can-tell-us-about-obesity-and-genetics/ In addition, it’s also likely that genes may not be directly responsible for obesity, but only be co-opted in the presence of certain environmental influences, like stress.
- What obesity research tells us about epigenetic mechanisms. Youngson NA, Morris MJ. Philos Trans R Soc Lond B Biol Sci. 2013 Jan 5;368(1609):20110337. doi: 10.1098/rstb.2011.0337. LINK
- Dietary factors, epigenetic modifications and obesity outcomes: Progresses and perspectives. Milagro FI, Mansego ML, De Miguel C, Martínez JA. Mol Aspects Med. 2012 Jul 4. LINK
- Interplay of early-life nutritional programming on obesity, inflammation and epigenetic outcomes. Martínez JA, Cordero P, Campión J, Milagro FI. Proc Nutr Soc. 2012 May;71(2):276-83. doi: 10.1017/S0029665112000055. Epub 2012 Mar 6. LINK
- Diet induced epigenetic changes and their implications for health. McKay JA, Mathers JC. Acta Physiol (Oxf). 2011 Jun;202(2):103-18. doi: 10.1111/j.1748-1716.2011.02278.x. Epub 2011 Apr 19. LINK
- Corticotropin-releasing hormone exerts direct effects on neuronal progenitor cells: implications for neuroprotection. Koutmani Y, Politis PK, Elkouris M, Agrogiannis G, Kemerli M, Patsouris E, Remboutsika E, Karalis KP. Mol Psychiatry. 2013 Mar;18(3):300-7. doi: 10.1038/mp.2012.198. Epub 2013 Feb 5. LINK
Estrogen and Endocrine Disruptors
- American Chemical Society (2007, August 20). Revealing Estrogen’s Secret Role In Obesity. ScienceDaily. Retrieved April 11, 2013, from http://www.sciencedaily.com/releases/2007/08/070820145348.htm
- Environmental estrogens and obesity. Newbold RR, Padilla-Banks E, Jefferson WN. Mol Cell Endocrinol. 2009 May 25;304(1-2):84-9. doi: 10.1016/j.mce.2009.02.024. Epub 2009 Mar 9. LINK
- The estrogenic endocrine disrupting chemical bisphenol A (BPA) and obesity. Vom Saal FS, Nagel SC, Coe BL, Angle BM, Taylor JA. Mol Cell Endocrinol. 2012 May 6;354(1-2):74-84. doi: 10.1016/j.mce.2012.01.001. Epub 2012 Jan 10. LINK
- Developmental exposure to endocrine-disrupting chemicals programs for reproductive tract alterations and obesity later in life. Newbold RR. Am J Clin Nutr. 2011 Dec;94(6 Suppl):1939S-1942S. doi: 10.3945/ajcn.110.001057. Epub 2011 Nov 16. LINK
- Female mice are protected against high-fat diet induced metabolic syndrome and increase the regulatory T cell population in adipose tissue. Pettersson US, Waldén TB, Carlsson PO, Jansson L, Phillipson M. PLoS One. 2012;7(9):e46057. doi: 10.1371/journal.pone.0046057. Epub 2012 Sep 25. LINK
- Low Dose Organochlorine Pesticides and Polychlorinated Biphenyls Predict Obesity, Dyslipidemia, and Insulin Resistance among People Free of Diabetes.Lee D-H, Steffes MW, Sjödin A, Jones RS, Needham LL, et al. (2011) PLoS ONE 6(1): e15977. doi:10.1371/journal.pone.0015977 LINK
- Obesity and persistent organic pollutants: possible obesogenic effect of organochlorine pesticides and polychlorinated biphenyls.Dirinck E, Jorens PG, Covaci A,Obesity (Silver Spring). 2011 Apr;19(4):709-14. doi: 10.1038/oby.2010.133. Epub 2010 Jun 17. LINK
- Endocrine disruptors and obesity: obesogens.García-Mayor RV, Larrañaga Vidal A, Docet Caamaño MF, Lafuente Giménez A.Endocrinol Nutr. 2012 Apr;59(4):261-7. doi: 10.1016/j.endonu.2011.11.008. Epub 2012 Feb 1. LINK
Sleep, Rhythms and Stress
- A molecular clock regulates angiopoietin-like protein 2 expression. Kadomatsu T, Uragami S, Akashi M,PLoS One. 2013;8(2):e57921. doi: 10.1371/journal.pone.0057921. Epub 2013 Feb 28. LINK
- Stress, visceral obesity, and metabolic complications. Kyrou I, Chrousos GP, Tsigos C. Ann N Y Acad Sci. 2006 Nov;1083:77-110 .LINK
- Sleep and obesity. Beccuti G, Pannain S.Curr Opin Clin Nutr Metab Care. 2011 Jul;14(4):402-12. doi: 10.1097/MCO.0b013e3283479109. LINK
- Chronic stress and obesity: a new view of “comfort food”. Dallman MF, Pecoraro N, Akana SF,Proc Natl Acad Sci U S A. 2003 Sep 30;100(20):11696-701. Epub 2003 Sep 15. LINK
- Stress and obesity: the role of the hypothalamic-pituitary-adrenal axis in metabolic disease. Bose M, Oliván B, Laferrère B. Curr Opin Endocrinol Diabetes Obes. 2009 Oct;16(5):340-6. doi: 10.1097/MED.0b013e32832fa137. LINK
- The hypothalamic–pituitary–adrenal axis and sex hormones in chronic stress and obesity: pathophysiological and clinical aspects.Renato Pasquali. Ann N Y Acad Sci. 2012 August; 1264(1): 20–35. doi: 10.1111/j.1749-6632.2012.06569.x LINK
- The Hypothalamic-Pituitary-Adrenal Axis, Obesity, and Chronic Stress Exposure: Sleep and the HPA Axis in Obesity. Eliane A. Lucassen and Giovanni CizzaCurr Obes Rep. 2012 December; 1(4): 208–215. doi: 10.1007/s13679-012-0028-5. LINK
- Chronobiology, endocrinology, and energy- and food-reward homeostasis. Gonnissen HK, Hulshof T, Westerterp-Plantenga MS. Obes Rev. 2013 May;14(5):405-416. doi: 10.1111/obr.12019 LINK
Vitamin D and Sunlight
- Causal relationship between obesity and vitamin D status: bi-directional Mendelian randomization analysis of multiple cohorts.Vimaleswaran KS, Berry DJ, Lu C, et. al. PLoS Med. 2013 Feb;10(2):e1001383. doi: 10.1371/journal.pmed.1001383. LINK
- Modest reversal of metabolic syndrome manifestations with vitamin D status correction: a 12-month prospective study. Al-Daghri NM, Alkharfy KM, Al-Saleh Y, Al-Attas OS, Alokail MS, Al-Othman A, Moharram O, El-Kholie E, Sabico S, Kumar S, Chrousos GP.Metabolism. 2012 May;61(5):661-6. Epub 2011 Nov 8. LINK
- Seasonal changes in the interactions among leptin, ghrelin, and orexin in sheep. Kirsz K, Szczesna M, Molik E, Misztal T, Wojtowicz AK, Zieba DA. J Anim Sci. 2012 Aug;90(8):2524-31. doi: 10.2527/jas.2011-4463. Epub 2012 Jul 10. LINK
- Hypovitaminosis D and incidence of obesity: a prospective study.González-Molero I, Rojo-Martínez G, Morcillo S, et al. Eur J Clin Nutr. 2013 Feb 20. doi: 10.1038/ejcn.2013.48. LINK
- “Is the Gut Microbiota a New Factor Contributing to Obesity and Its Metabolic Disorders?,”Kristina Harris, Amira Kassis, Geneviève Major, and Chieh J. Chou, Journal of Obesity, vol. 2012, Article ID 879151, 14 pages, 2012. doi:10.1155/2012/879151. LINK
- Supplementation of Lactobacillus curvatus HY7601 and Lactobacillus plantarum KY1032 in Diet-Induced Obese Mice Is Associated with Gut Microbial Changes and Reduction in Obesity. Park DY, Ahn YT, Park SH,PLoS One. 2013;8(3):e59470. doi: 10.1371/journal.pone.0059470. Epub 2013 Mar 21. LINK
- Lactic acid bacteria contribution to gut microbiota complexity: lights and shadows. Pessione E.Front Cell Infect Microbiol. 2012;2:86. doi: 10.3389/fcimb.2012.00086. Epub 2012 Jun 22. LINK
- Obesity and the gut microbiota. Flint HJ. J Clin Gastroenterol. 2011 Nov;45 Suppl:S128-32. doi: 10.1097/MCG.0b013e31821f44c4. LINK
- Functional interactions between the gut microbiota and host metabolism. Tremaroli V, Bäckhed F. Nature. 2012 Sep 13;489(7415):242-9. doi: 10.1038/nature11552. LINK
- Programming of host metabolism by the gut microbiota. Bäckhed F. Ann Nutr Metab. 2011;58 Suppl 2:44-52. doi: 10.1159/000328042. Epub 2011 Aug 12. LINK
- Lipotoxicity: effects of dietary saturated and transfatty acids. Estadella D, da Penha Oller do Nascimento CM, Oyama LM,Mediators Inflamm. 2013;2013:137579. doi: 10.1155/2013/137579. Epub 2013 Jan 31 LINK
- The interplay between the intestinal microbiota and the brain. Stephen M. Collins , Michael Surette & Premysl Bercik. Nature Reviews Microbiology 10, 735–742 (1 November 2012) | doi:10.1038/nrmicro2876. LINK
- Lymphotoxin regulates commensal responses to enable diet-induced obesity. Vaibhav Upadhyay, Valeriy Poroyko, Tae-jin Kim, et al. Nature Immunology, 2012; DOI: 10.1038/ni.2403. LINK