Our diet can massively affect our life span, period. It can increase our risk of disease, speed up the progression of cancers, heart disease, diabetes and other life threatening conditions. It is pretty essential we understand and know how to control our levels of inflammation, and dietary choice is one of them.
Diet, inflammation and stress have numerous implications to overall health, and what we eat, what we are exposed to, and what we avoid can have influential effects on conditions such as oxidative stress, sympathetic activity, transcription factors, and stimulation of pro-inflammatory pathways. The links between stress, inflammation and diet are never ending and they could all affect each other, but for the purpose of this article, I am going to solely focus on the dietary implications alone. Cancer, cardiovascular disease and diabetes account for 70% of the death in the US, and the common factor here is inflammation.
Firstly, what is inflammation? Inflammation is a physiological response to various tissue damage and infection. It initiates pathogen killing, tissue repair, and helps restore homeostasis at infected and damaged sites. Out of control, chronic inflammation can contribute to the perpetuation and progression of disease. This is why it is very important, not just via dietary practice, to control inflammation and reduce it where we can, and if anti-inflammation is necessary (sometimes inflammation is a desired response)
There are various diets that cause pro-inflammatory responses (the bad kind) and these include; refined carbohydrate, high sugar (HFCS), high saturated and trans-fat, low anti-oxidant, low omega-3, and low fibre diets. For the majority of the population, people are likely exposed to multiple of these factors and so the potential for inflammation is going to be extremely high. It is proven that inflammation increases our risk of metabolic syndrome, which is the starting point of so many health conditions/diseases. [1]
The science, if you are interested. If not, skip to the conclusion.
Refined Carbohydrates/Sugar:
Studies prove that lower glycemic index foods result in lowered levels of C-Reactive Protein, and IL-6, an inflammatory cytokine [2]. Not only this, but the same studies proved higher anti-inflammatory effects with those diets lower in processed, refined starches. This proves that diets high in refined carbohydrates will promote higher levels of inflammation, and could potentially result in many of the aforementioned conditions. There has been numerous studies on the effect of sucrose, fructose, HFCS and glucose and their respective effects on inflammation. Nationwide Food Consumption Surveys (NHANES) have suggested that the percentage of sweeteners from high-fructose corn syrup (HFCS) increased from 16% in 1978 to 42% in 1998, and then stabilised [3]. This tells us that the consumption of HFCS has exponentially increased over the last 4-5 decades and has meant that the products we buy and consume in modern social life, have a much greater impact on our health and level of inflammation. Much of the literature points toward fructose being the demon here, and many of the trials done with glucose actually see some improvements in inflammatory markers, when fructose consumption is replaced by glucose, albeit this study was done on patients with hepatic fat percentage greater than 8 [4]. To conclude on refined carbohydrates impact on inflammation, we can see that fructose is potentially the culprit, and that foods, and now most drinks have very high levels of HFCS could be the reason inflammation elects it’s effects via dietary intake of specific CHO.
Saturated and Hydrogenated Fats:
There are masses of data showing high-fat (saturated/trans) promote endotoxin translocation into the bloodstream [5]. Lipopolysaccharides, an endotoxin and probably the most inflammatory compound known to man, will wreak havoc if they are able to penetrate the gut lining and enter the bloodstream. This would result in a huge response from the innate immune system causing high levels of inflammation to try to counteract the foreign invader. It has been in the last few decades that scientists have actually understood the relationship between the immune system and the nervous system, as before they were thought to be independent. Its no surprise they are interlinked when we see the same chemicals (Interleukins) have different roles in each of the respective systems. If we activate the immune system, we will also activate the SNS, and this will actually help the initial innate response, but too much of a chronic exposure will evidentially be detrimental to our immune function. I went slightly off topic there, but back to dietary practice, we see that saturated fats and hydrogenated fats will make our inflammation levels rise due the role they play in increasing the density of LPS and even mimicking their role. The consequent response of the immune system will cause inflammation levels to rise dramatically.
Alcohol:
This will play a similar role to the previously mentioned fats in the effect on the microbiota and LPS. In most individuals, the adverse levels of LPS can be kept in check by the liver detoxification pathways. These pathways, especially in phase 2 can be, and are commonly overwhelmed by the actions of phase 1 and its exposure to multiple toxins. Alcohol, being an added, unwanted toxin, that has to be processed and removed by the liver, is just another burden to the organ, and potential impairment of liver detoxification pathways will inhibit the ability to remove high levels of LPS.
Another response from alcohol is going to be the direct damage alcohol has on cells. When cells die, they need to be removed and re-generated. Most of the time, when these cells can’t be recycled properly, the waste products from cells get dumped into the cytoplasm, instead of being removed properly, and this leads to more inflammation. Alcohol metabolism also directly leads to the production of free radicals, known for their ability to stimulate activation of a key inflammation transcription factor, nuclear factor-κB. [6]
Conclusion:
It is clear that refined carbohydrates, including manufactured goods like white bread, cereals, sugary drinks, sweets and so on, promote higher levels of inflammation. It is no help that these are the foods that are so readily available and convenient in todays society, and so no wonder so many people are now at such higher risk of disease like CVD, T2B and cancers than ever before. Other dietary choices like saturated fats and trans fats can have a huge implication on our internal inflammation too, so avoiding things like processed meats, limiting animal products to a sensible quantity (I’m still a fan of red meats, due to their numerous other benefits). Trans-fats like canola oil, takeaway foods, frozen foods, and other cakes, pies and baked goods will also have a large influence on our body inflammation, leading to a much higher risk of early mortality. Alcohol is an obvious one, and one that I hope many people conciously try to control the intake of, from all standpoints including calorific content, toxicity and as we have just discussed, inflammation and the consequently risk of contracting numerous diseases.
Luke French | Health & Physique Coach
www.lukefrench.co.uk
[1] Monteiro R, Azevedo I. Chronic inflammation in obesity and the metabolic syndrome. Mediators Inflamm. 2010;2010:289645. doi:10.1155/2010/289645
[2] Buyken AE, Goletzke J, Joslowski G, et al. Association between carbohydrate quality and inflammatory markers: systematic review of observational and interventional studies. Am J Clin Nutr. 2014;99(4):813-833. doi:10.3945/ajcn.113.074252
[3] Marriott B.P., Cole N., Lee E. National estimates of dietary fructose intake increased from 1977 to 2004 in the United States. J. Nutr. 2009;139:1228s–1235s. doi: 10.3945/jn.108.098277
[4] Jin R, Welsh JA, Le NA, et al. Dietary fructose reduction improves markers of cardiovascular disease risk in Hispanic-American adolescents with NAFLD. Nutrients. 2014;6(8):3187-3201. Published 2014 Aug 8. doi:10.3390/nu6083187
[5] Cani PD, Amar J, Iglesias MA, et al. Metabolic endotoxemia initiates obesity and insulin resistance. Diabetes. 2007;56(7):1761-1772. doi:10.2337/db06-1491
[6] Gloire G, Legrand-Poels S, Piette J. NF-kappaB activation by reactive oxygen species: fifteen years later. Biochem Pharmacol. 2006;72:1493–1505
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