"No such thing as a ‘Bad’ Food": Incorrect
A common phrase you hear a lot of ‘health professionals’ use. There is no such thing as a good or bad food. Bless them, they are just trying to follow the trend. This phrase would be correct if it read “there is no food that can interfere with short term weight loss”. I think that’s what these people are trying to get at, because all they talk about is a calorie deficit. Well, I don’t know about you, but I actually care for my clients long term biological health, and not if they just lose weight this week or not. So here is why some foods should actually be labelled bad foods in my opinion. But please, if you do approach this belief to fat loss, please use my previously stated quote “there is no food that can interfere with short term weight loss”.
Our nutrient quality has a profound influence over our biological function, and can alter the internal environment of our bodies, much to do with our health outcomes and our pursuits of fat loss. “No such thing as a bad food” is a very misleading phrase, and one that should not be floating around the industry in friggin' 2021.
Now you may have heard of the term ‘oxidative stress before’ and this is what can cause a fair amount of damage to our insides. There are plenty of easy ways to cause this, but for this article, we will stay on the nutrition side of things. There are numerous nutritionally mediated ways to induce oxidative stress, triggering inflammation. Oxidative stress, thus inflammation, is one of the main contributors to multiple human diseases. Short term, post-prandial mitochondrial oxidative stress causes inflammation. Extensive research has shown that high-glucose and a high-fat diets mediate inflammation, which suggests that oxidative stress may alter cellular physiological processes 
The prevalence of obesity has doubled since 1980 to 2008, which is extremely concerning. In that time the convenience and consumption of such foods like high sugar and saturated fat has been excessive. There is no surprise that the increase in this way of life has resulted in the obesity epidemic, where more than 50% of people in the WHO European Region are overweight . So if someone says a pizza, saturated (get it?) in processed foods and a high sugar dessert isn’t “bad” and won’t cause weight gain - in the grand scheme of things - the last 30 years of scientific, retrospective literature would disagree.
The harmful effects of free Reactive Nitrogen Species (RNS) and Reactive Oxygen Species (ROS), collectively known as free radicals, cause biological damage, namely nitrosative stress and oxidative stress respectively. Nutrient choice, quality and quantity will have a huge say in the production of free radicals.
1. High Glycemic Foods (lots of sugar basically)
Sugar, or highly sugary foods have been consistently associated with diabetes, obesity, cancer and coronary heart disease . There will be many people you see on social media saying sugar is sugar, it’s just a calorie etc. “when we eat complex carbs we break it down to sugar, and it’s the same thing”. TRUE, you are not wrong. But the key thing to note is that complex carbs, maybe a low glycemic option, wasn’t just pure sugar, hence why it's not called that, and that’s the key. Sugar itself is known to increase inflammatory markers. However if we eat a carbohydrate, lower on the glycemic index, it will have other stuff in it to. Many complex carbs, for example potatoes are extremely nutritious. Now there are many nutrients that act as anti-inflammatories and anti-oxidants. It is the balance of these pro-inflammatory and pro-oxidative molecules, with the anti-inflammatory and anti-oxidative nutrients that mediates the oxidative and nitrosative levels. So if we eat a food high in sugar, with little else in, we will be tipping the balance in the from of oxidative stress. If we eat sugar in the form of complex carbs that hold multiple other, highly nutritious components, inflammation will be more likely mediated. Sugar is not sugar (well it is), glucose is glucose. BUT, what comes with it will determine the effects.
Many people nowadays are on a calorie controlled diet, meaning if they decide to 'save calories' for meals including high sugar, and little else, then they will be tipping the balance, and inducing inflammation. Having that calorie controlled diet and trying to work in more amounts of sugary, fatty and palatable treats will only reduce the ability to get adequate nutrients from the remainder of their calorie allowance. And no, 5 portions of fruit and veg is not ‘enough’ to mean you can have the rest of your calories from ice cream. It really is as simple as, the more fruit and veg the better (supposing the individual has no gastric issues involving certain vegetables).
It is no surprise that consuming such foods while also being in a caloric surplus will just accelerate these problems, but we must be aware that a calorie deficit doesn’t simply mean all the negative effects of “bad” food are diminished, and you would be a fool to think so. Because short term weight loss is so dependant on short term energy balance, people will label no food as ‘bad’ because no food will compromise weight loss in such a short window of time. But these same fools maybe don’t understand the wider concepts behind obesity. As long as they have made their client lose weight in the 12 weeks of coaching, they will get a good before and after photo, so their job is done. That individual is more likely to be at risk of the previously mentioned diseases than the individual that ate sensibly throughout a calorie controlled dieting phase. Obviously i’m not saying eat 100% “good” foods, but the people that abuse this concept, will find out later in life.
Excessive high caloric intake from either a high-carbohydrate or high-fat diet will cause more substrates to enter into mitochondrial respiration. Subsequently, the number of electrons donated to the electron transport chain may increase. Upon reaching a threshold voltage, extra electrons might back up at complex III with further donations to molecular oxygen, which produces high levels of superoxide . This is known as high-energy electron leakage, and superoxide is a from of ROS, being conducive to inflammation.
2. Excessive consumption of (Saturated) Fats:
Studies conducted with high-fat diets in human and animals have proven to increase oxidative stress. Various pro-inflammatory markers are consistently being linked to high saturated fat diets, once study showing a marked increase in a pro-inflammatory cytokine after just 2 weeks of a high fat diet, leading to weight gain and body fat mass increases. A lot of the same principles apply to high fat consumption just like the high sugar consumption, so I won’t repeat myself.
One thing to note in the case of fats however is that many fats are extremely healthy, and actually support mitochondrial function (where we produce all of our energy). I would hope people reading this do not categorise fats into one basket and say they all have the same effect. It is the saturated and hydrogenated fats that will induce inflammation and be detrimental to health and weight loss. Fats like polyunsaturated, EPA, DHA, ALA etc are essential and are needed to optimal biological function.
So, there are “bad” foods that create a toxic, inflammatory environment that will certainly not aid our pursuits of fat loss, but will undoubtedly compromise our health in the long run, and potentially increase the likelihood that such individuals will end up with obesity, diabetes and heart diseases, the exact opposite of the initial goal; to improve health and body composition.
 Tan BL, Norhaizan ME, Liew WP. Nutrients and Oxidative Stress: Friend or Foe?. Oxid Med Cell Longev. 2018;2018:9719584. Published 2018 Jan 31. doi:10.1155/2018/9719584
 World Health Organization. Data and Statistics. The Challenge of Obesity-Quick Statistics. 2017.
 Schwingshackl L, Hoffmann G. Long-term effects of low glycemic index/load vs. high glycemic index/load diets on parameters of obesity and obesity-associated risks: a systematic review and meta-analysis. Nutr Metab Cardiovasc Dis. 2013 Aug;23(8):699-706. doi: 10.1016/j.numecd.2013.04.008. Epub 2013 Jun 17. PMID: 23786819.