The 11 Keys to Weight Loss 

1. Counting calories is unhelpful

Have you noticed how some people never seem to put on weight yet others look at food and gain weight? If they both ate the same calories, clearly something different is going on inside their bodies. Research has found the difference is their microbiome (gut bacteria). Different types of bacteria are more or less efficient at extracting calories and nutrients from the food we eat. We can predict obesity with 90% accuracy by studying your stool microbiome. Researchers can make skinny mice fat by changing their microbiome whilst keeping their diet and activity regime the same. This is why same calories cause different results in 2 people.

For long term weight loss we need to change your microbiome, then we will naturally stay lean even if we eat more. Starving yourself might work in the short term but if you yo-yo diet, that is, rapidly lose weight through a low calorie diet then put on weight by going back to your normal diet (or “cheating”) then back to low calorie, over time it will make your basal metabolism slower. It’s also not sustainable for most people.

Intermittent fasting can be useful in certain situations, as can a Fasting Mimicking diet like ProlonTM (that we offer some patients for other health issues). However, for weight loss, generally we suggest a new lifestyle that has clear stages of progression. That way you can stick to it, know what to do and when, and understand why it’s working for you.

Our approach lets you eat until you are full, and eat a wide variety of foods.

Over time you can introduce more and more foods. With our dietary plan you’ll re-set your hunger signals so your brain starts to recognise when you are full, you will stop craving sweet things, have more constant energy and blood sugar levels, and have greater endurance then ever before. The quality of calories is far more important than the quantity, so we never count calories.

2. You can’t exercise your way out of obesity


To burn this small handful of grapes (420kJ/100kcal) you would need to run for 9 minutes straight or walk for 26 minutes straight!  
Exercise though great for other reasons, isn’t the answer for weight loss.
See more examples of what 100 calories of food looks like here

What does it take to burn 100kcal with exercise?

3. Being overweight has nothing to do with willpower

Certain foods are addictive, and the latest Australian research shows that people with obesity don’t get the same brain signals that would normally make them feel satisfied after a meal, so they keep eating.

New drugs are trying to target this pathway but the reality is they are like using a Band-Aid on a broken bone. They can never change the incredibly complex gut microbiome or simultaneously impact the countless pathways and signals in the body. A drug is not the answer.

Research has now discovered that gut hormones enter the brain, and some are in fact produced in the brain itself, and these influence cognitive (mental) ability.[1] In addition, well-established regulators of synaptic plasticity, such as brain-derived neurotrophic factor, can function as metabolic modulators, responding to peripheral signals such as food intake. In other words, our mind and body are one[2].

4. Our brain and gut are one

Have you ever been anxious and felt the need to go to the toilet? Our levels of stress affect the gut and vice versa. Have you ever felt emotionally down and craved junk food? Recent research has demonstrated that neurotransmitters like the “flight or fight” stress hormones play a significant role in gastrointestinal function. Norepinephrine, epinephrine, dopamine, and serotonin have recently been a topic of interest because of their roles in the gut physiology and their roles in gastrointestinal and central nervous system diseases like Parkinson’s and Inflammatory Bowel disease[3]. Your gut "enteric" nervous system has around 500 million neurons and produces half your body’s Dopamine and 90-95% of your serotonin! (A common anti-depressant drug is an SSRI – Serotonin Reuptake Inhibitor that is designed to increase levels of this important chemical in the brain. Why not instead focus on where 90% is made, the gut?)

Neuroscientists now suggest that preventing the loss of masticatory function (ability to chew by keeping your teeth) will help "stabilize or even improve cognition" in the general population as well as patients with dementia[4]. Your mouth and brain are connected in far more complex ways that most people realise!

Our comprehensive program is the solution you’ve been searching for.

Studies have shown that what we eat directly impacts the gut microbiome (the ecosystem of different microorganisms in our digestive tract) and this can have profound impacts on our overall health.

Gut microbes communicate to the central nervous system through at least 3 parallel and interacting channels involving nervous, endocrine, and immune signalling mechanisms. The brain can affect the community structure and function of the gut microbiota through the autonomic nervous system, by modulating regional gut motility, intestinal transit and secretion, gut permeability, and potentially through the luminal secretion of hormones that directly modulate microbial gene expression. Evidence now points to alterations in this brain-gut-microbiome communication as being responsible for irritable bowel syndrome, obesity, and several psychiatric and neurologic disorders. [5] What we eat changes the gut microbiome. Our microbiome creates many of the key nutrients we need and changes the neurotransmitter levels in the body. Recall that 90% of your serotonin is made in the gut!

Wouldn’t it make sense then to focus on gut health when thinking about the rest of the body? At Evergreen Doctors we do. But we also go beyond that. We look at your diet, your emotional stress, your hormone balance, toxins, obesogenic chemical load, nutritional needs and unique genetics.

Together we create a customised approach and a step by step action plan.

5. Modern fruit is full of sugar and damages the health of animals

The Age reported in 2018 that selective breeding has made the fruit we eat so full of sugar, that Melbourne Zoo has had to wean its animals off it. "The issue is the cultivated fruits have been genetically modified to be much higher in sugar content than their natural, ancestral fruits,” says Dr Michael Lynch, the zoo’s head vet. "It's interesting. After doing a lot with nutrition here, I tend to eat less fruit." “Pretty much all cultivated varieties at present are sweeter than their wild counterparts,” says Dr Senaka Ranadheera, a food scientist at the University of Melbourne. "For example, wild apples are smaller and more bitter than modern cultivated varieties." Dr Ranadheera said there were reports of some fruits, such as plums, almost doubling in soluble sugar content in the past 20 years.” [6]
Newsweek also reported that the Zoo had found the fruit made the animals fat and rotted their teeth.[7]

Why is there so much confusion around what works for weight loss?

An interesting article in the Journal of Insulin Resistance said "The sugar industry has a long history of co-opting scientists. A team at the University of California, San Francisco, have discovered the paper trail of influence by the Sugar Research Foundation to exonerate sugar and divert attention to saturated fat as a cause of cardiovascular disease (CVD) in 1967, and to divert attention away from sugar as a cause of dental caries in 1971. Since then, those in the sugar, high-fructose corn syrup, beverage and processed food industries have paid for scientists’ complicity in marketing sugar as healthy. More recently, an analysis of Web of Science citations from 2008 to 2016, which searched for Coca-Cola conflicts of interest regarding funding, identified 779 articles.”[8] Many people in the media have likened industry’s resistance to the implementation of a sugar tax to the behaviour of the tobacco industry in the past when they tried to delay health warnings about smoking.

Furthermore, it’s very hard to perform studies because people tend to under report the bad food they eat and over report the good food. Frequently studies also use different definitions of low carbohydrate” or “good fat” or even the definition of “red meat”! Large differences in environmental exposures and lifestyle also confound studies. The greatest challenge though is that most research is done by large corporations with a vested interest in the outcome.

Slowly but surely, independent studies are being done now and they are proving again and again that the low fat approach is flawed. Eating less calories and exercising more won’t work in the long term. You know first hand that’s true.

6. Eating Fat doesn’t cause you to become fat

The world is increasingly waking up to the fact that eating fat can actually make you thin. Fat though high in calories is processed differently by the body than other fuel sources and tends to make you feel full. It also burns slower so you have more consistent energy throughout the day. Many ultra-endurance athletes now use fat as their fuel rather than carbohydrate gels and snacks. Even peak sports teams are now embracing this new paradigm as their performance is increased by it.

We are witnessing an epidemic of obesity and diabetes because people are eating food that they are not genetically designed to eat. Your ancestors never ate most of what we consider “food” in our modern age. Importantly, neither did people living in your country in the 1950s. It’s only really since the 1960s that our diet has dramatically changed, and that has paralleled the increases in cancer, diabetes and obesity. At the same time we’ve been exposed to thousands of toxins and chemicals that are now being shown to build up in our bodies over decades and cause all sorts of problems.

More and more studies are showing that to lose weight, eating fat can actually help. However, it needs to be in conjunction with eating the right amounts of proteins and carbohydrates. Fat alone won’t make you thin, but the entire approach will.

The good news is it means our weight loss approach includes plenty of tasty food including cream, butter, eggs, nuts and meat. (If you are vegan you can still use this approach, it’s simply modified to be plant based).

When the food guidelines were introduced they encouraged people to eat a low fat diet, this meant they had to increase their carbohydrate intake as a proportion of their calories.  This has had disastrous consequences to our health and clearly those guidelines do the opposite of what they were intended to achieve. Food consumption patterns changed, and so did the rates of obesity. A decade or so later diabetes started going up as well.

The Early Childhood Longitudinal Study, (Birth Cohort), was a representative sample of US children that found low fat intake leads to obesity. 10,700 children were examined at age 2 and 4. Across racial/ethnic and socio-economic status subgroups, 1% (skim milk) drinkers had higher BMI scores than 2% (whole fat milk) drinkers. “Increasing fat content in the type of milk consumed was inversely associated with BMI score (p<0.0001)… children drinking 1% skim milk at both 2 and 4 years were MORE LIKELY to become overweight/obese between these time points."[9]

7. Eating Fat doesn’t cause coronary heart disease

National dietary guidelines were introduced in 1977 and 1983, by the United States and United Kingdom governments, with the ambition of reducing deaths from Cardiovascular disease by reducing or modifying fat intake. Australia soon adopted similar approaches and so began the war on fat.

At the time of researcher Zoë Harcombe’s PhD thesis, no analysis of the evidence base for these recommendations had been undertaken. Her PhD examined the epidemiological and Random Control Trial (RCT) evidence available to the US and UK regulatory committees at their respective points of implementation. The thesis also examined the epidemiological and RCT evidence available currently, to assess if the guidelines are supported at the present day. Dr Harcombe conducted four systematic reviews and meta-analyses of the RCTs and epidemiological evidence available, firstly, at the time of introducing the guidelines, and secondly, now, examining the relationships between dietary total and saturated fat, serum cholesterol and all-cause or CHD mortality.

Her results indicate that 6 RCTs (including only 2,467 males – most of whom had already had a heart attack) published prior to 1983 were available to the dietary guideline committees: 5 secondary prevention studies and 1 including healthy subjects.

There were no differences in all-cause mortality and non-significant differences in Coronary Heart Disease mortality, resulting from the dietary interventions. In other words there was no evidence that a low fat diet would reduce heart attacks or all-cause mortality.[10]

None of the studies themselves recommended a low fat diet based on their results. In fact 3 of them concluded NOT to use a low fat diet to avoid heart attacks!

Similarly, 6 epidemiological studies available to the committee at the time of the dietary guidelines did not find any relationship between all-cause and coronary heart disease mortality and dietary saturated fat.

Dr.Zoe Harcombe described the famous 7 Countries study as “the lowest possible form of evidence”, and a review of the original data found a much stronger correlation between latitude and heart disease than cholesterol levels, possibly pointing to vitamin D deficiency being the real cause of those heart attacks.

Including more recent RCTs and epidemiological studies  (including the Women’s Health Initiative study) in the analysis did not change the findings of No Effect. Even if an effect had been evident, most studies included only males, who had pre-existing heart disease, making results difficult to generalise to the greater, healthy population.

Dr Harcombe concludes that government dietary fat recommendations were untested in any trial prior to being introduced and current evidence does NOT support the current low fat dietary guideline. The modern dietary guidelines have been a mass experiment with the populations’ health and the result has been disastrous. Health authorities don’t understand the problem is the very core hypothesis the original recommendations were based on were flawed, so it’s no wonder that people are getting fatter and sicker following them. It’s time to re-evaluate the evidence and adopt a new approach.

A recent study found that lowering cholesterol with plant sterols can be harmful to your health![11] Modern studies are pointing to things like smoking, trans-fat, high blood pressure, and diabetes as the cause of heart disease, not saturated fat.

Dietary cholesterol does NOT increase blood cholesterol in most people.[12] Dietary fat may increase blood cholesterol in some people (while decreasing triglycerides), but this increase does not relate to increased Cardiovascular risk or mortality risk possibly due to reduced atherogenic cholesterol particles, and increased antiatherogenic particles.[13]

For decades the standard for assessing arterial disease and heart attack risk has relied predominantly on monitoring blood risk factors, with low density lipoprotein (LDL) levels considered the ultimate marker of risk.  However, the coronary artery calcification (CAC) score is a more direct measure and far superior as an indicator of atherosclerosis and cardiac event risk. In comparison to the CAC score, the LDL level appears to be a very poor indicator of heart attack risk and potentially even misleading[14]. Studies have found that despite increasing CAC scores (patients who are at high risk of having a heart attack), they can have similar LDL levels to people who are low risk.

Very Low Carb Ketogenic Diet (VLCKD) vs Low Fat Diet (LFD)

8. When you eat matters - it impacts your weight Set Point

It’s well known that your body tends to hold your weight within a certain range. You can lose a little easily but more than that is hard and the body tends to easily put that weight back on. Like a thermostat the body’s metabolism actually changes up and down burning more or less calories in the background (your basal metabolic rate) to maintain this range or fixed “Set Point”. Chrono-Nutrition research has recently found that by eating at the right time of the day you can create a new set point in the brain.[15] For long term weight loss to be successful, we need to change that set point, then you become a “naturally” thin person who’s body works against weight gain. This is how naturally skinny people can eat a lot and not put on weight, they have a different Set Point compared to overweight people who easily put on weight.

9. Fat tissue is not just spare padding – it’s a source of hormones!

Adipose tissue (fat) is no longer considered to be an inert tissue that just stores fat in the body. It is now known to be an endocrine organ. Adipose tissue is responsible for the synthesis and secretion of several hormones that control nutritional intake (leptin, angiotensin), control sensitivity to insulin and inflammatory process mediators (tumour necrosis factor α (TNF-α), interleukin-6 (IL-6), resistin, visfatin, adiponectin, among others) and pathways (plasminogen activator inhibitor 1 (PAI-1) and acylation stimulating protein (ASP) for example).[16] This is a big part of why being overweight increases the risk of thrombotic disorders contributing to endothelial dysfunction and, subsequently, to accelerated atherosclerosis.[17]

Within fat tissue, enzymes such as aromatase and aldo-keto reductase 1C are responsible for metabolizing testosterone into estrogen and 5-dihydrotestosterone into inactive metabolites. Adipose tissue can also affect the secretion of gonadotropin, which influences the formation of androgen in the testes. This is why many overweight men develop “man boobs”, may lose hair and feel less confident in themselves. Their testosterone is being converted to estrogen because of the fat! This then feeds back and higher estrogen causes more fat to be deposited. Furthermore, androgens regulate the activity of lipoprotein lipase, a key enzyme involved in intracellular esterification of adipose tissue. When this mechanism is interfered with adipose tissue becomes dysfunctional.


10. What you eat matters!

After a single sugary meal the blood vessels in your body get damaged. The picture below is an electron microscope view of the inside of a blood vessel. The thin threads are the Gylcocalyx layer, which when damaged results in LDL cholesterol being more able to damage the blood vessel wall and turn into an atheroma[18].

A multi-centre study in the USA found that what you eat also makes a major difference to your energy expenditure (the amount of calories you burn) and the hormones that regulate hunger!

Change in total energy expenditure was 209 kcal/d greater in those assigned to the low carbohydrate diet compared with the high carbohydrate diet! Ghrelin and Leptin were significantly lower in participants assigned to the low carbohydrate diet compared with those assigned to the high carbohydrate diet, meaning that by eating the right diet, your hunger signals and metabolic hormones work for you, helping you stay skinny long term.[19]

Other toxins and inflammatory chemicals such as TNF-α promote early atherosclerosis by increasing transcytosis of LDL across the deeper cells (endothelial)[20].

Thus inflammation can turn a potentially harmless level of LDL in the blood into a dangerous atheroma in the wall of the blood vessel, that could lead to strokes and heart attacks.

11. Surgery is NOT a great solution

Surgery like gastric sleeves causes permanent nutritional deficiencies that require lifelong daily supplementation of calcium citrate, vitamin A, K, D, B1, B12, iron, folic acid, copper, and thiamine.

The surgery in essence is designed to stop you absorbing your food properly. The idea is by removing half your stomach you will feel full after eating less food, but this alone is often not sufficient to bring about long term weight loss as the stomach stretches and if the nutritional, toxic, hormonal and emotional components are ignored the weight will be put back on.

After surgery if careful attention isn’t paid to nutritional supplements, it’s possible to develop osteoporosis and serious nutrient deficiencies. Best practice is to check levels of key nutrients with a blood test every 6 months though often this isn’t done. The operations are almost always permanent as well.

Obesity becomes a feed-forward loop

Rather than spending $20,000+ on a radical operation or trying another fad diet, get your weight sorted permanently by working with us. We believe your body wants to be well, and is holding onto the weight for a reason. Given the right weight loss program, you will lose the weight and naturally return to a state of wellness.


[1] Mittal, R., Debs, L.H., Patel, A.P., Nguyen, D., Patel, K., O’Connor, G., Grati, M., Mittal, J., Yan, D., Eshraghi, A.A., Deo, S.K., Daunert, S., Liu, X.Z. (2017, September). Neurotransmitters: The critical modulators regulating gut-brain axis. Journal of Cellular Physiology, 232 (9): 2359-2372. Doi: 10.1002/jcp.25518.

[2] R.A.F. Weijenberga, E.J.A. Scherdera, F. Lobbezoo Neuroscience and BioBehavioural Reviews 35 (2011) 483-497


[4] Gibbons, A. (2007, June 15). Paleoanthropology. Food for thought. Science, 316(5831) : 1558-1560. Doi: 10.1126/science.316.5831.1558.

[5] Gomez Pinilla F. Brain Foods: the effects of nutrients on brain function. Nature Reviews Neuroscience 2008;7:568-578



[8] A. Malhotra, G. Schofield, RH. Lustig, The science against sugar, alone, is insufficient in tackling the obesity and type 2 diabetes crises – We must also overcome opposition from vested interests, Journal of Insulin Resistance ISSN: (Online) 2519-7533, (Print) 2412-2785 [Link]

[9] Arch Dis Child. 2013 May;98(5):335-40. doi: 10.1136/archdischild-2012-302941. Longitudinal evaluation of milk type consumed and weight status in preschoolers. Scharf RJ1, Demmer RT, DeBoer MD

[10] Harcombe, Z., Baker, J.S., Cooper, S.M., Davies, B.,Sculthorpe, N., DiNicolantonio, J.J., Grace, F. (2015, February 1). Evidence from randomised controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983: A systematic review and meta-analysis. Open Heart, 2(1). Doi: 10.1136/openhrt-2014-000196

[11] Zoë Harcombe and Julien S. Baker, Plant sterols lower cholesterol, but increase risk for coronary heart disease, DOI : 10.3844/ojbsci.2014.167.169, OnLine Journal of Biological Sciences, Volume 14, Issue 3, Pages 167-169, [Link]

[12] Demasi, M., R.H. Lustig, and A. Malhotra, The cholesterol and calorie hypotheses are both dead—it is time to focus on the real culprit: insulin resistance. Pharmaceutical Journal doi, 2017. 10.43.

[12] DuBroff, R., Cholesterol paradox: a correlate does not a surrogate make. BMJ Evidence-Based Medicine, 2017. 22(1): p. 15-19.

[13] Halton, T.L., et al., Low-carbohydrate-diet score and the risk of coronary heart disease in women. New England Journal of Medicine, 2006. 355(19): p. 1991-2002.

[14] Erbel R., Lehmann N., Churzidse S., Rauwolf M., Mahabadi A.A., Möhlenkamp, S., Moebus, S., Bauer, M., Kälsch, H., Budde, T., Montag, M., Schmermund, A., Stang, A., Führer-Sakel, D., Weimar, C., Roggenbuck, U., Dragano, N., Jöckel, K.H., Heinz Nixdorf Recall Study Investigators (2014, November 7). Progression of coronary artery calcification seems to be inevitable, but predictable - results of the Heinz Nixdorf Recall (HNR) study. European Heart Journal, 35 (42):2960-71. Doi: 10.1093/eurheartj/ehu288.

[15] Nathan Rose BHSc(Nat), Clinical Education Manager at Metagenics, research presented at ACNEM Conference 2019

[16] M. Coelho, T. Oliveira, R. Fernandes, Biochemistry of adipose tissue: an endocrine organ, Arch Med Sci. 2013 Apr 20; 9(2): 191–200. Published online 2013 Feb 10. doi: 10.5114/aoms.2013.33181

[17] Hutley L1, Prins JB., Fat as an endocrine organ: relationship to the metabolic syndrome, Am J Med Sci. 2005 Dec;330(6):280-9, [Link]

[18] "Arterial glycocalyx dysfunction is the first step in the atherothrombotic process" QJ Med 2008; 101:513-518

[19] Ebbeling, Feldman, Klein, Effects of a low carbohydrate diet on energy expenditure during weight loss maintenance: randomized trial, BMJ 2018; 363 doi:

[20] “TNF-α promotes early atherosclerosis by increasing transcytosis of LDL across endothelial cells: Crosstalk between NF-κB and PPAR-γ” Investigative Ophthalmology & Visual Science, August 1994, Vol. 35, No. 9