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naturenurturenutrition-blog · 9 years ago

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An (Anti-)Inflammatory Post

TL;DR

inflammation is as beneficial as it can be destructive over time

short-term inflammation is a protective mechanism, part of immunity

long-term inflammation (chronic low-grade systemic inflammation) is detrimental to overall health

chronic inflammation has been noted to quietly underlie conditions including (but not limited to) obesity, diabetes, heart disease, stroke, and various cancers

eat lots of (anti-inflammatory) plants

and lots of colors

cut it out with all the (pro-inflammatory) solid & saturated fats

get your body up and moving.

you don’t need an exercise regimen. just wiggle yourself for a few minutes a day and you’ll be a healthier person.

sleep soundly. sleep regularly. sleep comfortably.

and check out my future-post about circadian rhythms :)

Inflammation

...is a topic I find fascinating. The scientific community has taken an interest as well. You may have noticed gastroesophageal reflux disease trending on Facebook—not only because it is such a high-fashion topic to begin with but also because researchers have linked the condition to the inflammatory process, as opposed to the previous suspected culprit (stomach acidity). So what good is inflammation, if any? Why do we experience inflammation at all? Protective as it is destructive, beneficial as it can be detrimental—the following post will detail the process of inflammation, including its purpose, its mechanisms, and the damage done under conditions of chronic low-grade systemic inflammation. If interested additionally, sources have been numbered and can be provided upon request. :)

Chronic Low-Grade Systemic Inflammation

Okay, so let’s start with a little bit of background information. Not much, but we’ll go pretty far back. Millions of years ago, developing complex life was forced to face threats to their survival. Organisms which succeeded were able to pass on genetic material while those unable to thwart such threats did not—part of evolution. External threats to complex life (predators, availability of food, etc.) were compensated for with adaptations through natural selection (camouflage, speed, heightened senses, etc.). However, overcoming internal threats, like bacteria and viruses, requires a different mechanism. This mechanism is called immunity, fine-tuned over the ages to fend off pathogens through an intricate system of communication between body cells and participating enzymes, which recognize and eradicate intruders using methods including but not limited to cytokine-release and phagocytosis, (10). The result was, then, (and continues to be) a complex life form capable of self-defense from the inside out. From humans to houseflies (which to this day share many of the same mechanisms for protection) innate immunity plays a pivotal role in survival.

This invaluable process of immunity is referred to as inflammation. Various inflammatory components, such as Tumor Necrosis Factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1ß (IL-1ß), monocytes, lymphocytes (natural killer cells, T cells, B cells), and macrophages, among others, do their best to work together to protect the body.

The general mechanism behind inflammation helps to heal injuries and fend off pathogens by calling attention to areas of the body which are deemed compromised. This is a critical point. In the short-term, this is necessary for survival—“flagging” the area with cytokine-releases, which are recognized by macrophages (“big-eaters”), which then infiltrate area to big-eat invaders, resulting in eradication of the threat. However, it has become apparent in recent years that chronic low-grade systemic inflammation, caused by genetic and environmental factors including but not limited to the impact of diet, has negative effects on overall health—both prompting the onset and perpetuating many of the chronic diseases plaguing the population of the Western world. This is fascinating to me as it is worrisome as it is promising. This condition perpetuates itself with good intentions, through positive feedback loops which essentially do more harm than good. The immune system flies under its own radar—“can’t see the forest for the trees”, so to speak. Though generally not diagnosed as a condition itself, chronic inflammation has been noted to quietly underlie conditions including (…but not limited to) obesity, diabetes, heart disease, stroke, and various cancers. It has been suggested, then, that a reduction in chronic inflammation through multifactorial interventions could reduce the severity and prevalence of existing conditions, as well as the incidence of new cases.

Systemic Inflammation in Relation to Chronic Health Conditions

Chronic low-grade systemic inflammation is characterized by a constantly active innate immune system, resulting in high circulating levels of various biomarkers, including, most notably, tumor-necrosis factors, interleukins, and C-reactive protein (CRP). TNF-α and IL-6 are cytokines produced by macrophages and adipose cells to initiate protective cascades throughout the body. CRP is an example of a protein produced in a response to these cytokines. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are also produced in greater quantities, causing oxidative stress* and damage while activating some of the same pathways initiated by TNF-α and IL-6, such as inducing gene transcription factors that code for further production of TNF-α, IL-6, and IL-1ß, (6)(7). This positive feedback loop characteristic of chronic inflammation poses a threat to overall health. Prolonged exposure to dysregulated inflammatory factors can cause confusion amongst body cells, including hyperproliferation (read: lots of cell division due to upregulation of transcription factors, and resultant genetic mutation) and vascular dysfunction (due to accumulation of proinflammatory cells in the subendothelial space), (3)(7). These and other complications of a prolonged inflammatory state contribute to many chronic health conditions whose incidence are on the rise.

Obesity and Chronic Inflammation

Obesity is recognized as a state of chronic inflammation, (5). By definition. Adipose cells produce inflammatory cytokines (“adipokines”), like TNF-α and IL-6, constitutively—that is to say, these cytokines will be expressed even without direct need or purpose, (5). Thus, high levels of visceral (body) fat contribute to greater levels of circulating cytokines. Obesity is considered a precursor to many health conditions, such as cardiovascular disease, which could be attributed to this proinflammatory impact on the body, (1). Multifactorial intervention (discussed later) could help lower levels of circulating adipokines, thus reducing risk of further complication.

Pain, obesity, and inflammation — Chronic pain is often associated with high body mass index (BMI). Obese men and women experience higher rates of pain than those of normal weight, even when accounting for other pain conditions, (1). This association strengthens with age. While often discounted as mere mechanical pain one might expect with bearing excess weight, the pain conditions seen among the obese population include pain in the upper extremities, thoracic spine, and neck, as well as conditions such as fibromyalgia, osteo- and rheumatoid arthritis, neuropathy, and migraine headaches, (1). Many of these pain conditions are not associated with the mechanical hardship of extra weight, but are, in fact, seen in correspondence with high concentrations of inflammatory biomarkers in the blood. Considering the tendency of obesity (through adipokine action) to stimulate and perpetuate the positive feedback loop associated with inflammation, inflammatory pain conditions among the obese population are not all that surprising. Understanding this link could provide physicians and affected individuals a method of treatment previously unexplored.

Insulin Resistance and Chronic Inflammation

Research indicates that chronic inflammation and insulin resistance may be closely related. Insulin resistance is associated with increased production of proinflammatory cytokines TNF-α and IL-6, which play a key role in systemic inflammation, (5). In fact, upregulation of TNF-α and IL-6 are considered pivotal to the association between obesity and insulin resistance, (5). When present secondary to obesity, insulin resistance increases the risk of heart disease, type 2 diabetes, and stroke—all also associated with chronic inflammation, (1). Another inflammatory condition, osteoarthritis, was observed in a 20-year study by Schett and colleagues of over 900 patients, which concluded that type 2 diabetes (characterized by insulin resistance) could be considered an independent predictor of severe osteoarthritis leading to joint replacement, (1). Considering the results of this study alongside the classification of osteoarthritis as an inflammatory condition, credence is lent to claims linking inflammation and insulin resistance.

Cancer and Chronic Inflammation

Cancer does not present in adult animals, even with dominant oncogenes, unless triggered by injury and tissue regeneration, which is mediated by the inflammatory response as the body heals, (7). It is important to note that inflammation can be pro- or antitumorigenic, but an inflammatory microenvironment is considered essential to the growth of all tumors, (7). Different inflammatory components play different roles during the initiation, promotion, conversion to malignancy, invasion, and metastasis of tumor cells, (7).

Pathogens which promote tumor growth may recruit host immune cells to prompt a persistent response in a given area—initiation, (7). This provides the basis for an environment in which the initiated tumor can thrive. Inflammatory cells produce ROSs and RNIs, which have the ability to damage DNA and cause genomic instability (‘oxidative damage’), (7). The inflammatory microenvironment and its constituents (cytokines, tumor-associated macrophages, ROSs, RNIs, and more) also increase mutation rates by inactivating mismatch repair enzymes within a cell’s nucleus and inducing immunoglobulin gene class switching, (7). This is important to note, as many cancers require four to five gene mutations before becoming genetically prepared to compete with neighboring cells as a tumor, (7).

Following development, the inflammatory environment will promote angiogenesis (‘genesis’ of blood vessels) in an attempt to provide the area with a route for the body’s defenders to travel, thereby thwarting “non-self” cells. However, immunosurveillance (the ability of the defenders to distinguish self from non-self) is depressed in a tumor-promoting microenvironment—thus, this effort provides the tumor with nutrition necessary to continue hyperproliferation, (7). Should the tumor outgrow its nutrient and oxygen supply, necrosis will occur, prompting an even greater inflammatory response accompanied by even greater blood vessel generation, cytokine production (calling for additional resources), and growth factor recruitment, (7). While the immune response is warranted, this action promotes growth. The newly generated blood vessels also allow the tumor a path to spread, should it metastasize, (7). Thus, while an inflammatory microenvironment is a healthy component of the healing process, the chronically inflamed individual could see detrimental effects associated with a positive feedback loop of inflammatory mediators in terms of tumor initiation and promotion. Reducing inflammation could be protective against tumorigenesis.

Cardiovascular Disease and Inflammation

Inflammation and cardiovascular disease are strongly associated, which is related to the ability of inflammatory compounds to increase vascular permeability (ability of plaque to take implant within the blood vessel) and atherosclerotic plaque instability (ability of plaques to break free of the blood vessel—traveling through the bloodstream, potentially blocking arteries or causing strokes), (3)(8). Monocytes and T-lymphocytes, immune cells which carry cholesterol, have the potential to implant themselves in the endothelial lining of blood vessels, causing hardening and narrowing of arterial walls known as atherosclerosis, (3). Compounds associated with oxidative stress, such as ROS, RNS, and free radicals, increase lipid oxidation and the likelihood of atherosclerotic plaques, (6). Higher circulating levels of immune compounds increase the likelihood and frequency of this occurrence, while other inflammatory mediators, such as interleukins and adhesion molecules, increase plaque vulnerability and instability, (3). This endothelial dysfunction associated with inflammation is highly predictive of cardiovascular events, (8). Chronic inflammation leading to cardiovascular disease presents as a dangerous comorbidity to other systemic conditions, such as diabetes and renal disease, (8).

Treatment of Chronic Inflammation

Strategies for reducing chronic low-grade inflammation often employ multifaceted treatment plans to target the underlying issue contributing to this systemic condition. This could be different per individual. Such strategies often call for dietary and behavioral changes, alongside possible pharmaceutical intervention.

Fruit and Vegetable Consumption

Fruits and vegetables contain many beneficial compounds like vitamins and antioxidants, such as vitamin C and ß-carotene, which are related to lowering markers of inflammation and oxidative stress, (6). Polyphenolic compounds found in produce are used by plants to protect against various stressors, such as pathogens and UV light, and it is speculated that these compounds continue to be protective in the human body when ingested, but further research is needed, (6). Studies have shown that consumption of fruits and vegetables in adults is inversely related to risk factors associated with cardiovascular disease, including markers for inflammation and oxidative stress, (6). The link between markers of inflammation and atherosclerosis is well established in adults, but few studies have been conducted on the diets of healthy children to determine how inflammation, diet, and age are related. One such study, conducted by Holt, Steffen, Moran, Basu, Steinbergr, Ross, Hong, and Sinaiko (2009) evaluated the adolescent diet in conjunction with markers of inflammation (CRP, IL-6, TNF-α) and oxidative stress (prostaglandins and metabolites, ROS) in order to further understand the impact of fruit and vegetable intake on the body throughout adolescence. The researchers found that total fruit and vegetable intake, excluding french fries and juices, are significantly inversely related to circulating levels of CRP, TNF-α, IL-6, and F2-isoprostanes (a marker of oxidative stress), (6). They conclude that diets rich in antioxidants, flavonols, and folate from fruit and vegetable sources are associated with lower levels of inflammatory markers and oxidative stress, which begins in early life and could lower cardiovascular risk as the individual ages, (6).

Cruciferous vegetable intake — A study conducted by Jiang and colleagues (2014) evaluated the diet of 1005 Chinese women, age 58.1±8.8 years, in order to determine the effects of cruciferous vegetable intake on markers of inflammation. Results of their study indicate that increased intake of cruciferous vegetables is associated with lower blood concentrations of TNF-α, IL-1ß, and IL-6 in females, (2). The association was stronger among women who did not have a medical history of inflammatory diseases or persistent infections, (2). The researchers associate the antioxidant and anti-inflammatory properties of these cruciferous vegetables—chiefly bok choi, green cabbage, Chinese cabbage, cauliflower, and white turnips—to the reduction in circulating cytokines, (2).

Dietary Fat Intake

Concern about intake of dietary n-6 polyunsaturated fatty acids and its resultant impact on chronic inflammation has become a topic of discussion within the scientific community. The basis of this lies in the connection between arachidonic acid and subsequent synthesis of proinflammatory eicosanoids, such as prostaglandin E2, (4). While this is a known phenomenon associated with linoleic acids, a review of current literature, including 15 studies with dietary intervention involving dietary linoleic acids, indicates that “virtually no evidence” is available to support the claim that dietary n-6 polyunsaturated fatty acids contribute to increases in inflammatory markers such as CRP, cytokines, and adhesion molecules, among others, (4). It is also noted that, though eicosanoid synthesis is prompted by arachidonic acid, the result is a product which can be used for pro- and anti-inflammatory purposes within the body, (4).

Saturated fat intake seems to negatively impact chronic inflammation. Saturated free fatty acids in the blood stream cause lipoapoptosis and production of TNF-α, followed by activation of NF-κB in macrophages, which is part of the positive feedback loop associated with high concentrations of circulating cytokines, (5). This suggests that elevated blood and tissue lipid concentrations are related to the immune response responsible for chronic inflammation, (5).

The Mediterranean Diet

In a study conducted by Casas and colleagues (2014), the effects of the Mediterranean diet (MD) on markers of vascular wall inflammation by forming three groups for intervention and comparison: MD+extra virgin olive oil (EVOO), MD+nuts, and low-fat diet. For twelve months, participants adhered to their randomly assigned diet, and biomarkers were assessed at completion as they had been before the intervention began. Following intervention, it was found that CRP and IL-6 were reduced “45% and 35% and 95% and 90% in the MD+EVOO and MD+nuts groups, respectively, (P<0.05, all) compared to low-fat diet control,” (3). The intervention also lowered blood pressure among the MD groups, and reduced concentrations of LDL cholesterol by 5% in the MD+EVOO group and 8% in the MD+nuts group, but the authors state that these changes are insufficient to explain the reduction of risk for CHD, instead pointing to a reduction to the body’s inflammatory reaction as the cause for risk reduction, (3). The authors believe this helps provide an explanation for previous studies which note that subjects at high risk who follow the Mediterranean diet are less likely to experience cardiac heart disease, stroke, and mortality, (3). While blood pressure and circulating LDL are reduced relatively quickly with the Mediterranean diet, extended adherence is associated with greater impact on inflammatory markers versus short-term dieting, (3).

Behavioral Intervention

The association between BMI and biomarkers of inflammation and oxidative stress is moderately strong, suggesting that changes to diet in conjunction with increased physical activity could lead to weight loss, which has been noted to considerably decrease oxidative stress in obese men and women and to reduce CRP and IL-6, (6)(1). Considering obesity’s link to inflammation and the role of adipocytes in cytokine production, a modest reduction in visceral fat could reduce circulating cytokines and lessen the impact of chronic inflammation, (1). While it may be difficult to begin such an exercise regimen as an obese individual, Dr. Robert A. Bonakdar remarks in his article about obesity-related pain, “Post-exertional soreness does not represent long-term worsening of pain conditions,” (1). It is also noted that a review of literature provides that moderate exercise does not increase the progression of osteoarthritis, a common pain condition, (1). A healthy, regular sleeping pattern is also recommended. Sleeping dysregulation and depression are both thought to intensify the symptoms of obesity, (1). IL-6 is linked to each of these, as well as progression of osteoarthritis, (1).

Nutritional Concerns

Nutritional concerns associated with systemic inflammation beyond those posed by the chronic conditions it underlies include some nutrient deficiencies. One such nutrient is vitamin D. Vitamin D deficiency has been linked to inflammatory conditions such as rheumatoid arthritis and inflammatory bowel disorder, (8). Low vitamin D status is also significantly correlated with higher blood concentrations of markers of inflammation CRP and IL-6, as well as markers of oxidative stress, (8).

Another nutrient of interest is iron. In a study conducted by Tussing-Humphreys, Liang, Nemeth, Freels, and Braunschweig (2009), the diets of adolescent females were analyzed to determine how excess adiposity and inflammation impact iron status. The researchers found that heavier weight girls had significantly higher levels of CRP, accompanied by higher rates of iron deficiency, (9). Other factors, such as dietary iron and vitamin C intake, menstruation, and physical activity were not significant predictors of deficiency in this sample, (9). This data suggests that inflammation perpetuated by excess adipose tissue contributes to insufficient iron status, (9).

RECAP

Chronic low-grade systemic inflammation is a condition underlying many of the chronic diseases we are familiar with, including obesity, cardiovascular disease, and diabetes. Cytokines and other factors of immunity are prompted for synthesis by way of gene activation and cell signaling, resulting in a self-perpetuating positive feedback loop that becomes detrimental to overall health given time. Chronic inflammation is known to accompany obesity and could explain the link between high BMI and insulin resistance. It is also associated with tumor initiation, growth, and metastasis. It is well established that chronic inflammation underlies the vascular dysfunction which leads to atherosclerosis. Systemic inflammation is also linked to nutrient deficiencies, such as vitamin D and iron. For these reasons and others, understanding how to prevent chronic low-grade systemic inflammation may wll be critical to optimizing health. Pharmaceutical measures, such as NSAID regimens and BCAA supplementation, can be employed, but a mostly plant-based diet low in saturated fats is also effective. This reduction in inflammation through diet is attributed to the antioxidant power of vitamins, minerals, and polyphenol compounds found within the foods, in conjunction with their replacement of potentially higher fat, less nutrient dense options. Behavioral interventions, such as increasing physical activity and sleep regularity also contribute to lower circulating levels of inflammatory biomarkers.

If you also find inflammation interesting and have any questions or concerns (or just want to talk an ear off/want your ear talked off about it), feel free to get in touch :) Thanks for reading. Love you — I mean, bye

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naturenurturenutrition-blog · 9 years ago

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Schrodinger’s Blog

Perhaps now, after my post about genes and nutrition (nutrigenomics) and another about environment and nutrition (gastrointestinal flora, the microbiome, millions of pals, what have you) you have noticed that nutrition is crazy. It makes perfect and absolutely no sense on an individual basis, like almost everything and nothing else does, respectively. So I’m going to throw a brief curveball in terms of subject continuity and talk about something else so very subjective, but also concrete and maybe the ulterior motive for the entire blog—body image.

Disclaimer: Please forgive me for my word choice throughout. I am making an effort to be honest but careful. I also, in this blog and in my life, am moving toward an attitude of non-judgement, but you cannot possibly understand how ingrained these thought patterns can be. Or, perhaps you do, and in that case, I am sure I don’t need to ask for your forgiveness :) Thank you for reading.

I, like many before me and many to come, have struggled with my body image for several years—maybe all of the memorable ones. I grew up in a family with a father who was compelled to comment on every female figure as it related to his interest. Loudly. In front of my mother, his wife. In front of my brother, who would learn from him. In front of me, his daughter. My mom would often chime in—further admiring or admonishing the women, for reasons I actually can understand. Her playful acceptance masked a deeper pain. Through nature or nurture (hey, that’s the name of th—), these are qualities I recognize within myself. The competitive environment, unfair standards and ideals, and my subsequent weight gain (in sharp contrast) made for a bumpy road out.

I’m sure it seems at this point that I feel as though my childhood is to blame for my current self-perception. This is not the case. It is a factor, but there are many factors. What I really believe is that, during maturation, there are days that feel like waking up. Like coming online as a human. Like, “What was I doing before this?” I’d say I’ve had upwards a dozen of these phase-shifting sort of moments, and maybe I can only speak for myself. Regardless, the accompanying insights have been enlightening or debilitating—or both, or both intermittently. I don’t feel like a victim, but I also can’t say I never did. My mom and I have discussed these topics in detail, and I believe we’ve both come to a place of understanding. It’s not like it has been easy for either of us. I also don’t blame or feel resentment toward my dad, but rest assured I’m not afraid to set him straight nowadays. Anyway.

From an obese adolescent to an adult of healthy weight, there have been many hurdles along the way in terms of goal achievement. One goal I’ve yet to fully achieve is that of positive body image—although I am making progress every day. While I am generally happy with myself at this point, my pride is related to my accomplishments—not necessarily the ‘product’ I see when I look in the mirror. I’ve spent time trying to reword my last sentence into something that seems justifiable to someone without body image issues but 1) anyone who does suffer similarly will know exactly what I mean and 2) that’s part of the problem: it does not particularly make sense. While I feel a warm sense of accomplishment, my goals are ever-shifting—as goals should, in the sense that progress is continuous—but boy, sometimes the thought of contentment is just as sweet as it is seemingly impossible to come by (or ‘settle for’, depending on what type of day you catch me). Other times, and thankfully more frequently lately, I catch glimpses of it. They are becoming less fleeting.

I would like to take a moment to mention that my body image, at times, has been majorly, even directly, correlated with my weight. Not solely, but it has certainly been a major factor. This is a flaw in logic. For so long, I chased societal ideals of beauty. I still do. But it is not necessarily because I, myself, find them ideal. I have been working to discern what I personally feel is appropriate and ‘ideal’ for myself. It’s health—physically and mentally. I will discuss this a bit more later. I would also like to highlight that the consequences are far beyond “:( Not feelin’ so good today.” If you know me personally, I may have alluded to my tendency to pick at my skin. This is a severe but lessening tendency. Not too far in the past, I would sit for half-hours at a time, picking at the skin of my legs, arms, and face. This is a symptom of body dysmorphic disorder, I would later learn (repetitive behavior). Since becoming aware, my habits have lessened (including the urges), but they have not completely dissipated, nor have I completely reconditioned myself. It is hardly as simple as committing to quit. It is an involved process of restructuring subtle, damaging thought patterns that, until now, have occurred subconsciously.

So, I say all that, to reiterate this—body image is overarching. Body image can mean the difference between greeting each day with joie de vivre and literally dreading the thought of crossing the threshold of the bedroom door. It is anxiety over the fixed. It is a series of thoughts and behaviors which reinforce insecurities, encourage isolation, prompt doubts and fear, and amplify every negative thought about self-worth.

elice how is this related to nutrition

i mean i get it but why

i will tell you

We are born impressionable. And we are taught to think of ourselves all wrong. Consider this portion of a lecture delivered over 50 years ago by the incredibly astute Alan Watts (or, skip below where I summarize):

“…The European Dissociation: the conception of man as an unhappy amalgamation of mind and body, spirit and matter, ego and not-ego, subject (knower) and object (known). And this concept of man has very curious consequences—I’ve mentioned a lot of them—but one that strikes me more and more is that it’s a non-participative conception of man. By that I mean, it causes us to feel ourselves as observers of life, whether that life is inside our own bodies or whether it’s outside in the external world—we’re observers. We are the subjects and all that is the object—and, that is to say, it confronts us, it stands over against us. And we’re looking at it. And, in a way, this is symbolized in our whole way of life in so far as its end object seems to be to confront the television screen, which is non-participative contemplation of something which has been impoverished in its material and physical reality—deprived of, say, touch and smell and taste and so on. And so, because we have great expectations out of this contemplation, whether it be of television or of mundane existence, but we’re not with it—you see, we don’t believe we are our bodies. We say 'I have a body’ and we say 'I have instincts'—we never say 'I am a body’ or 'I am instincts.’ And the bodies we allow ourselves to have are a little bit pseudo, I mean—they’re elegant surfaces, the ideal body is, […] it’s an elegant surface, but it’s not supposed to secrete sweat or tears, it’s not supposed to smell at all, it’s inside (?) so rather improper and one is expected to give it attention in a sort of aloof way but spend one’s life, on the whole, being as unconscious of one’s body as possible. Alright then, so, we have a conception of ourselves which is estranged from our physical organism, and therefore our whole life is estranged.”

Alright then, so, we have a conception of ourselves which is estranged from our physical organism, and therefore our whole life is estranged.

Alright then.

Not many things I’ve heard or read have resonated with me quite so.

The other day, I was lucky enough and so happy to attend a hot yoga class with my friend Kayla. It’s the first time we’ve ever made plans. I was actually pretty excited. To clarify, I say ‘actually’, not to detract from Kayla at all, but because it is unusual that I would look forward to plans. In fact, Kayla is great. We didn’t start off as friends, but that, then, was in fact a manifestation of my own body image issues. If you’ll recall, the theme is ‘overarching’. So very overarching, that I now consider the latter point—that I’m not excited about any plans, ever, on Earth—very closely related to my body image as well. I am working on it. ANYWAY I think, even way back then, I knew that we would get along pretty well. Our happy connection felt familiar even before it was fully established. So we had a great time! However, I could not help but feel, so acutely, the estrangement Watts refers to. I could feel the disconnect as my thoughts overpowered and, frankly, confused my body—myself. I recognize this estrangement now like I recognize that I was always friends with Kayla, like I learned to recognize the subconscious thought patterns that lead to my repetitive behaviors. Somewhere, I knew, but was not prepared or equipped for the knowledge that I am my body—every instinct, intuition, pleasure, and pain that accompanies life. However, years of misguidance and misunderstanding have allowed the feeling of estrangement, the make-believe fissure between body and mind, to manifest itself as a very real internal disconnect that allowed for the doubt about my organism despite the confidence of my mind. Growing up, I didn’t know how to call it by its right name, so I accepted my “clumsiness” (in many senses of the word) and added it to the list of things I could feel self-conscious about. Not only this, but body image issues related to this estrangement have created many additional struggles throughout my lifetime related to intimacy, of any and all varieties. So, during this class, all other variables controlled, I chased after myself in an attempt to catch up with my body and breath, realizing the truth behind that which Watts had said—I do not believe myself to be my body. I have always considered myself a “soul” of sorts (call it what you will), loaned a body. This body, my dumb body, uncoordinated and clumsy, was provided me in order to carry out my (the soul’s) dumb wishes, whatever those are.

How foolish.

A book I am struggling to finish kicks this idea up a notch, prompting the question: “Elice were you even paying attention when you were reading all that?” This book, Everything You Need to Know to Feel Go(o)d by neuroscientist Dr. Candace Pert, details the “psychosomatic network”. This is basically a descriptive term for the link between thought and behavior—rather, the lack of distinction—including elements such as memory and emotion, which operate off of feedback throughout the entire body (not just in the brain and spinal cord). I feel as though this is just another way of explaining Watts simplistic claim—I am my body. Dr. Pert explains that memories are stored all throughout the ‘bodymind’, that behaviors (think small rituals—mantras, even) can prompt feelings, and that changing an attitude can alter our actions. Again, to learn this was to hear what was familiar for the first time. Ralph Waldo Emerson would call it ‘genius’.

However, this enlightenment could only come of my misunderstanding: then, a very logical conclusion from a combination of factors, including but not limited to my upbringing, my weight fluctuation, and another point Watts alludes to: the one-dimensional impact of media. In Watts’ time, it was restricted to television. As a note, this guy was a serious visionary. Nowadays, the times have changed. Media is social. "Reality" is malleable to the poster and flatly presented to an audience, ready and waiting to (intentionally or otherwise) cast judgement through the filter of their own perception. This one-dimensional representation of ourselves and others as cardboard cutouts often serves to isolate, as we present ourselves as fraudulent personas or aspire, misguidedly, to those of others.

I would like, instead, to allow you in.

It smells something like lavender and spearmint in the room I’m writing in. I smell like some hippie smell called “Amber” from our local hippie-smell vendor, Scent From Heaven.

I taste coffee and dates. Back to smells, I also might have coffee breath.

I feel soft most everywhere but my knees, where the hairs are sorta prickly because I stopped shaving every day, and my forehead, where I am breaking out and trying not to pick at my skin. Also my hair feels fabulous from today’s baking soda/vinegar wash. Don’t mean to brag, it’s just true.

The light in the room is dim, primarily provided by a book light attached to the screen of my laptop.

It sounds like key-clicking and dog snores.

My body is me. I am here and alive. Your body is you, so are you. We are dimensional.

I have made an effort to remove all suicidegirls et cetera from my feed. I’m sorry, you’re beautiful, I know, but it’s just not beneficial for me, and, frankly, I do not know who it is beneficial for because all I can think of in the time that I am not subconsciously drawing comparisons between our every feature are guys like my dad. (Please take a moment to remember my disclaimer—this is a very difficult feeling for me to describe that is tangled up in years of misunderstood jealousy and hopelessness.) I would like also to say, I have been very happy to see pictures of my friends and acquaintances I know flaunting what they’ve got because I have aspired to the confidence I see in them in those photos, and how, for some of them, it is a real accomplishment—just like it would be if I would or could do the same. If you know me from other walks of life, you may have noticed me get salty about fitspo—this is because of its one-dimensional nature. A lot of folks leave a lot of things out. So, for these and other reasons, last month, I lost my marbles and did some not unthinkable things, but things I hadn’t thought of before. One of which I’ve mentioned: I have stopped shaving my legs every day because 1) I am blessed with light leg hairs, making the mental transition easy and 2) let’s just go ahead and paragraph break—

If I were to tell you that I feel comfortable leaving my home without makeup on, or in shorts without shaving, or without a bra or in my sweatpants, or without washing my hair, I would be lying. But the truth is that I like telling that part of myself to shut the fuck up. Because, if you’ll notice, I said 'leaving my home’ and that’s exactly what I meant to say. I could not comfortably enter the world without first preparing myself to societal standards. In addition to periodic shave-strikes, I have also made an effort to wash my hair less frequently, such that I would not feel obligated to shower—to ‘completely’ ready myself—each and every time I plan to leave the house. I am not one-dimensional. I am not the flatness of my appearance. My body image has, for so long, been tied to one dimension. I did not understand that my value is and must be multi-dimensional.

ELICE YOUR BLOG IS ABOUT NUTRITION WHAT ARE YOU DOING

I’m getting there, that’s what.

At yoga, our instructor helped us through the practice by explaining how the link between our thoughts and our movement is our breath. Anyone who has spent any amount of time with yoga could attest to this. This ‘link’ is what makes careful, focused (but also effortless, simple) breath so critical to the practice of yoga—it provides a concrete area of focus for the seemingly separate (the mentally separated) realms of body and mind to share and work together. However, I truly believe that they key here is discipline. So did our instructor. We held a chair pose for, like, seven or eight minutes (or maybe just 45 to 90 seconds, who could be sure). Discipline… discipline is something I have become familiar with. Not totally, not constantly, not in every area of my life but

to practice nutrition is discipline.

aha

Through this cultivation of discipline, and over several years (and still), I’ve learned self-respect, boundaries, patience. I’ve found control and lost it.

I don’t say this to suggest that those who don’t practice my idea of nutrition are undisciplined. But nutrition is my ticket. It requires interest. Time. In current society, it also usually requires an additional motivator. But nutritional discipline occurs at its own pace. The time that it has taken me to cultivate my own appreciation for nutrition has allowed me to learn a great deal about health, not only as it relates to healthy foods but also in terms of physical and mental well-being. And I have found reward in learning and practicing at greater depths.

Nutrition also provides another tool for me to use as I remove the psychological block I have created between myself and my acceptance that I am my body. It is the link which integrates and perpetuates the psychosomatic network. Using nutrition, changing my diet—with the idea that I am (very literally, in every sense) recreating myself through my food choices—has hardly been restrictive. It is liberating. I feel no sense of loss in turning away from the foods that once comforted me. What I have gained through nutrition is a brand new, perhaps the only sense of self I have known.

This is where I am compelled. It is my passion. Nutrition, for me, is not about meal plans. It is about defining your wellness and exploring it. If you struggle similarly, you may consider nutrition as an outlet but, more importantly, know that what you experience is relatable and you have a friend in me.

I hope this has been a multi-dimensional experience for you.

#nutrition #body image

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naturenurturenutrition-blog · 9 years ago

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The Deal with pre- and probiotics

so i get asked

elice

what’s the deal with pre- and probiotics

please tell us

we are dying

so I am going to spitball on the topic for just a blog.

First: microbiome = flora = bacteria. gastrointestinal = gut. I’ll be interchanging.

okay

I really like thinking about the topic of –biotics, particularly in relation to the ecosystem that is the gut.

It’s fun to think of. We move through the day imagining ourselves as one entity—a soul, a mind, a body, the union of all three, whatever—while hardly pausing to think of the millions of inhabitants, the hundreds of species that would call our bodies home if they could speak or write or fathom our existence. In fact, some of them perform invaluable services for us. Bacteria in the large intestines (like E. coli!) synthesize vitamins in the K family, which are blood clotting factors, for uptake and use by the body. Weird, right? Who knew. Other intestinal bacteria synthesize vitamin B12, cobalamin, which supports nerve and blood cell health. No big deal, right? Vitamin suppliers!! They also help digest food, and ward off pathogenic bacteria (thereby boosting immunity).

So at this point you are undoubtedly asking yourself, “Elice, how do I populate my body with nanobugs to do my bidding?” I will tell you.

If you haven’t yet considered it, ‘probiotic’ is basically the opposite of ‘antibiotic’.

That seems simple enough but took me a while to recognize.

While antibiotics work to rid your body of pathogens, probiotics work to colonize the gut with the live strain of your choosing. Neat, right?

Maybe. It’s not really clear how well this process works. Some foods are naturally considered probiotic (fermented foods) while others are made into functional foods through the addition of live strains to the product. Think of how many factors could influence the efficacy of probiotic functional foods: potential for improper handling (chiefly temperature), pH during various stages of digestion, enzymatic activity, preexistence of competitive bacteria in the gut—it becomes difficult to remove some of the confounding variables in order to study just how beneficial probiotic functional foods might be.

For this reason, I think probiotics may serve a very special function in the diet, particularly at times when the microbiome may be compromised including medical cases related to antibiotic use and diarrhea. Probiotics may serve to help repopulate the biome, so there are certainly situations where their application may be helpful (at least not-harmful).

Then there are prebiotics. Boy, do I love prebiotics. But let’s talk about them a little first.

Prebiotics serve to feed existing gut bacteria. I think of prebiotic functional foods as microbiome fortifiers. Prebiotics include some types of fibers (like fructooligosaccharides), and can be added to food items (making them “functional foods”) or can be found naturally within foods which may already be part of your diet. When you get to thinking about it, this is amazing. We know that insoluble fibers serve some chief functions within the body, such as decreasing gastrointestinal transit time as well as increasing stool bulk.

Sidebar—Don’t let yourself feel weird thinking about the topic of GI transit time and stool bulk. It’s really important. Studies suggest that increased GI transit time (i.e, the longer the food sits in the stomach and intestines) increases the risk for some cancers, particularly colon cancer. (That being said, increase your hydration status with your insoluble fiber intake—it is important when you consider that whole stool bulk thing J)

Okay okay so we learn that insoluble fibers serve some chief functions within the body, such as decreasing gastrointestinal transit time as well as increasing stool bulk. Otherwise, they are classified as fibers because our body is unable to break the darn things down. However—some of the bacteria contained within the microbiome can do exactly that!! Thus, these otherwise completely useless dietary components serve a very worthwhile purpose—feeding our tiny inhabitants—so we classify them prebiotics.

So, should you skip merrily across town with your new million best friends to go drink up/eat up all the prebiotic/probiotic functional foods you can find?

Here is my opinion, subject to change as science helps our knowledge base to evolve:

Probiotics can be added to the diet to potentially bolster beneficial bacterial growth within the gastrointestinal microbiome.

There is no contraindication for probiotic foods in a healthy population, with the exception of allergens like lactose and yeast, and those prescribed a low-FODMAP diet. (Severely immunocompromised individuals, the critically ill, and patients with short-bowel syndrome should consider the possibility of undesirable bacterial overgrowth.) It sounds like, if you’re seeking out probiotic products, you have your health in mind already. Don’t let labels trick you. Don’t spend too much money. Remember that there is still much science to be scienced, but do what makes you feel good.

Similarly, prebiotic functional foods are neat, but don’t let labels trick you and don’t spend too much money.

And finally, what I really, really think:

The best way to enhance your intestinal flora is to mindfully choose healthy, fiber-rich foods that you enjoy, thereby nourishing yourself while providing your microbiome buddies with a little something to munch on. Not only, then, are you improving and defining your diet [which, don’t forget, is specific to you and only you (and I guess maybe your million new friends)], you are very naturally encouraging the growth and decline of the species which should naturally grow and decline in response to your/their diet, without introducing competition (or spending a lot of money on the words “pre-“ and “probiotic” when, in reality, the fibers and the cultures are found naturally in quite a few foods).

. So, below, I will list some foods that could become new staples for you and/or all the wee ones which call you home:

Prebiotic foods (those containing fibers which are digestible to gut bacteria)

Onions

Garlic

Asparagus

Bananas

Soybeans

Artichokes

Whole-wheat foods

Probiotic foods (those containing active cultures)

o Fermented foods:

Yogurt

Kefir

Aged cheeses

Miso

Tempeh

Soy

Kimchi

Sauerkraut

KoMbUcHa

Pickles/pickled things!

:) Any questions?

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naturenurturenutrition-blog · 9 years ago

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Eat right ♥

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naturenurturenutrition-blog · 9 years ago

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naturenurturenutrition-blog · 9 years ago

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☝🏼️☝🏼☝🏼Focusing on real food instead of food-like products is one of the best things you can do for yourself.

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naturenurturenutrition-blog · 9 years ago

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Think health, not beauty. U beautiful anyway, baby <3

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naturenurturenutrition-blog · 9 years ago

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Nutrigenomics — the crux

There is one lecture from my undergraduate studies that stands out from all the rest, in that it truly rearranged the schema I had created for nutrition in my mind. That lecture focused on the topic of nutrigenomics.

Nutrigenomics

is, first and foremost, a real word. It is at the crosshair of genetics and diet. Nutrigenomics focuses on the interaction between the chemical components of an individual’s diet and his or her genes, at the genomic, proteomic, and metabolomic level.

…let’s start with some definitions. I used some research by Sales, Pelegrini, & Goersch to help me out.

Genes—hereditary molecules which dictate protein synthesis.

This indicates not only observable features but also aspects such as disease susceptibility. Thinking of genes in this way will help facilitate an understanding of the molecular interaction between DNA and dietary components. Speaking of…

Nutrigenomics—the use of biochemistry, physiology, nutrition, proteomics, metabolomics, genomics, and epigenomics to uncover and explain the molecular interactions between dietary components and genes

This science seeks to determine how “bioactive compounds” (dietary components) may affect gene expression, through propagation or suppression, and also involves study of protective nutritional factors in relation to the genome.

Epigenetics—exploration of the modification of DNA and proteins, and changes in chromatin structure without changing the sequence of nucleotides; carried out by chemical compounds which modify or ‘mark’ the genome in such a way that it can indicate cellular functions, including where and when to carry out such tasks (known as ‘epigenetic marks’)

Epigenomics—the study of the complete set of (all, basically) epigenetic modifications, from cell to organism

Epigenetic marks are passed from one cell to another during cell division. Thus, these marks are passed along genetically throughout generations.

“These signatures are influenced by genotype in the surrounding media (environment, diet, and drugs, e.g.) and will determine the phenotype.”

Proteomics—the study of the complete set of proteins involved in all biological processes

Transcription—DNA —> RNA

Transcriptomics—study of the complete set of activated RNA transcripts.

This area of study is essentially devoted to transcription factors, which (when activated) travel to and act upon DNA—either promoting or inhibiting transcription (upregulating and downregulating, respectively). Transcription factors behave like sensors, which act in favor of homeostasis. Transcription varies based on circumstance, such as physiological signals (including dietary components and their metabolites), hormones, drugs, disease states, and more.

Transcription practically regulates itself. Transcription factors dictate DNA activation, which guides protein synthesis; protein synthesis (guided by transcription factors through DNA activation) provides short amino acid sequences which not only act as substrates for larger protein structures, but also the inhibitory feedback mechanism indicating that a particular transcription factor in action should downregulate.

Consider, at this point, how external factors (ex: amino acid availability, body pH, etc) could throw cogs in the gears of this otherwise seemingly flawless system. Remember, too, that the cell has a life cycle of its own—conditions inside and functions of the cell will vary depending on its stage in the cell cycle. So much to consider!

Metabolomics—the area of genomic study devoted to changes in metabolites (primary and secondary ‘byproducts’), as well as metabolism under environmental and genetic disturbance.

This is particularly neat because metabolites are often quite functional—in fact, to refer to them as mere ‘byproducts’ is quite the misnomer. Metabolites can serve as substrates for future reactions or may act as inhibitory feedback molecules. Others are mere waste, produced through synthesis and macromolecule degradation.

What makes this relevant? Beyond the marvel that is the microscale teenyverse in which these biological processes are carried out, there is one even more amazing component of this equation—

we have a say in how it’s done.

Our genes provide a framework, but we get to help paint the picture. There are precious few ways our bodies are capable of communicating with our genes. While we cannot always control the quality of our environment or the physiological stressors which have the potential to set chemical cascades in motion and possibly causing our body detriment, those of us who are fortunate enough to be able to choose our diets have the ability to make protective choices each and every day. By protective choices, consider this: a diet higher in fruits and vegetables will provide nutrient-dense energy to the body alongside anti-inflammatory benefits. A system protected from the physiological stress imposed by inflammation will operate more readily at homeostasis than a body which is consistently fighting the stress of inflammation (through mechanisms as microscale as alterations in transcriptional factors, which dictate protein synthesis). Perhaps this is speculative, but it seems to me as though a body whose energy expenditure must be unduly directed to repairs due to stressors is not allowed the freedom, is not spared the effort, to better turn itself over in the direction of desirable, protective genetic expression. In any case, it is true that the molecules, the phytopigments, which comprise our foods become us as our bodies absorb their energy and colors and nutrients in order to carry out cellular processes, and the fabric of our being is forever changed.

It has been scientifically established and I’ve sort of tried to scratch the surface of the mechanisms driving the way that dietary constituents, carried throughout the body by the circulatory and lymphatic systems after absorption through the gastrointestinal tract following a meal, can make changes to genetic activation… thus altering protein transcription and translation… resulting in what is essentially A DIFFERENT FUTURE FOR THAT INDIVIDUAL BASED ON HIS OR HER GENETIC MAKE-UP AND DIETARY CHOICES!!! That may seem extrapolated, but, truly, by how much? This is the most amazing topic in the WORLD (…in the opinion of this observer).

So, in terms of protective benefits, this means: eat lots of colors (but not lots of red meats), eat fibers and vegetables and fruits and, for good measure, keep your carbohydrate intake consistent.

However, there is one interesting caveat—

our genetic difference between humans, our 0.1% genetic difference, is enough variance to cause nutritionally significant effects. How is this?

Just a few more definitions.

Single Nucleotide Polymorphisms (SNPs): change/replacement of one nucleotide; found in at least 1% of the population.

This sort of just means that the gene got it wrong! Interesting note, most are found outside of coding sequences (without effect on protein synthesis or function). There are different types of SNPs: Linked (outside of gene) and Causative (in gene). Causative SNPs can be coding (changes amino acid sequence) or non-coding (changes amount of protein produced).

Haplotype—set of SNPs that are generally inherited together

SNPs can be inherited! In groups!

Mutation: change to DNA sequence that noticeably alters protein synthesis

So, a causative SNP could be considered a mutation if its activity noticeable alters protein synthesis,

Variant: ‘mutation’ without noticeable alteration in protein synthesis

These microscale differences (SNPs) can have macroscale consequences. The example that resonates with me is one which was provided at a presentation delivered at my state’s annual Academy conference. I, an espresso enthusiast, perked my ears at the mention of a difference in caffeine metabolism related to a known and identifiable SNP in the genome. Between variants A and B in the human population, individuals with variant A (the majority) are characterized as slow metabolizers, while individuals with variant B (the minority) are homozygous recessive and considered fast metabolizers. This has implications for heart disease, as (according to a study conducted by Cornelis, El-Sohemy, Kabagambe, & Campos in 2006), for slow metabolizers, coffee intake may be associated with increased risk of nonfatal myocardial infarction, while—for fast metabolizers—coffee intake may even be protective up to four cups.

What this means is, scientifically, we have advanced to a point at which nutrition assessment may be conducted genetically. Meal plans may be individualized instead of generalized.

That study, in fact, makes a good case for this statement:

“As in pharmacogenomics, where a drug will have diverse impacts on different segments of the population, researchers recognize that only a portion of the population will respond positively to specific nutritional interventions, while others will be unresponsive, and still others could even be adversely affected.” —M. Nathaniel Mead, MSc

Sounds a little null but is actually really fuckin’ cool. The statement is tailored a little specifically for those interested in intervening nutritionally upon others, but, when you break it down a little (“digest” it, if you will), you see it indicates that food acts in tandem with genetic expression, and differently between individuals. The message of this statement—that there is no such thing as a one-size-fits-all nutrition prescription—lends credence to the otherwise vague catch-all that is the phrase “genetic predisposition”. He goes on to say, “Whether that genetic potential will eventually manifest as a disease depends on a complex interplay between the human genome and environmental and behavioral factors.” While dismissed by some, the concept of genetic predisposition is very true and real and actual and, such, may have nutritional consequences. Such consequences can be accounted for and even acted upon as the science of nutrigenomics develops.

Rather than invalidate existing or further research, the existence and significance of genetic variation allows for further research into the application of nutrition prescriptions.

How EXTREMELY exciting.

Can you imagine, would you enjoy an existence where you knew the precise genetic implications of your diet?

#nature #nurture #nutrition #nutrigenomics #genetics #gene expression #diet #DNA #RNA #transcription #SNP #inflammation #phytochemicals #vegetables #blog

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