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Phyto 
Diet Clinic

Why the Claudia Louch Customised Diet works

Causes for weight-gain, obesity and weight fluctuations: the principle of the Set Point Diet at the UK natural Diet Clinic.

How the phytoclinic natural weight loss diet works

Claudia Louch weight management works on the principle of leptin resistance; hence each patient undergoes not only rigorous health checks prior starting his or her diet. A crucial factor is the measurement of each patient’s leptin levels, which is performed by an independent laboratory blood test, and forms the very basis for each diet plan. Each patient receives his or her customised diet plan, depending on the health history, check-up outcome, life style and dietary requirements.

Steps of the natural dietary weight loss program include:

  • A patient questionnaire to be completed prior the appointment to determine each patient’s suitability for the diet
  • A first 1-hour consultation will establish the patient’s and his/her family’s health history
  • Anthropometrical measurements and other diagnostic tests will be undertaken via high-tech medical devices:
    • Height, weight, waist and hip circumference
    • BMI, Body Fat Percentage, Body Skeletal Mass Percentage
    • Resting Metabolic Rate
    • Pulsoximeter Blood Oxygen measurements
  • Spirometry Test
  • Blood Pressure and Pulse measurements
  • A comprehensive urine test, performed by an automated urine analyser, the results of which will be given to patients during the consultation.

All of this is an ancillary part of the consultation. Other investigations may be performed on site if deemed necessary depending on your health status.

*If you are unable to attend our clinic or live abroad you may be able to obtain a diet plan in the Design My Weight Loss Diet section.

Phyto Diet Clinic London Laboratory tests

A comprehensive blood analysis, including a leptin test, is mandatory and patients are referred to an independent London laboratory. Further test requests may depend on the case history evaluation during the consultation. The blood tests form together with the consultation the basis for the customisation of a patient’s diet.

*If you are unable to visit our practice or live abroad, you may, depending on your country’s regulations (please check with your authorities) be able to order the blood tests online in the Diagnostic Tests section.

Once all the data is collated and your suitability and health status has been fully assessed, Claudia will customise a personal diet plan for you.

Follow Ups

2-weekly follow-up appointments are mandatory throughout the duration of the diet. This is necessary to not only guarantee the success of the diet, but to monitor patient’s health status and talk through any issues, which may have arisen, as well as re-check anthropometrical measurements on a regular basis.

Upon completion of the diet patients will be referred to an independent laboratory for a comprehensive blood and leptin test, to compare their current health status from the start of the diet.

Upon successful completion of a diet program, patients will receive a maintenance diet for life.

How much weight loss may be achievable?

The average weight loss for female patients is 3kg (6. Pounds) within 2 weeks. The rate of weight-loss may vary and depends also on patient’s adherence and commitment to the diet. Men loose usually slightly more and may achieve on average a weight loss up to 5kg (11 Pounds) in 2 weeks. A steady rate of weight-loss may be maintained throughout the diet if the diet plan is followed as advised; each diet is customised for the patient’s needs and insures that all macro- and micronutrients are being supplied to the patient on a daily basis.

The diet does not restrict any food groups, unless requested specifically by the patient, as it is designed to improve long-term health. The Set-Point-Diet is not a fad-diet, but based on sound scientific principles, providing the human body with all the nutrients it requires on a daily basis.

What if I am a vegetarian or vegan or have any other personal food restrictions?

As each diet plan is customised for the patient it is possible to tailor the diet to dietary preferences and requirements.

Is there anything else I should know?

All questions will be discussed during the first and following follow-up appointments. Patients will also be given with an accompanying diet a fact-sheet, which will guide the patient through the diet.

Claudia Louch’s Dietary Approach at the UK phyto weight loss Clinic

Claudia Louch’s dietary approach is different to any other diet currently available, as her approach is rooted in the latest cutting edge science.

Prior to the discovery of the adipocyte hormone leptin, obesity was thought to result more from a lack of will power than from an underlying biological disorder. Now, 15 years after leptin's discovery, a much different picture of how obesity occurs is beginning to emerge. At its heart is evidence that consuming a high-fat diet induces inflammation in key neuronal systems that govern energy homeostasis, an effect that increases the defended level of body weight.

The discovery of the link between feeding, hypothalamic inflammation, and the control of body weight is rooted in the study of how insulin resistance. This develops when tissues are exposed to a supply of nutrients that exceeds their energy requirements. In muscle, liver, fat tissue, and the vasculature, sustained exposure to excess nutrient intake induces cell inflammation via multiple mechanisms. In addition to the recruitment and activation of immune cells in fat tissue of obese individuals, nutrient excess can also induce inflammation via cell-autonomous mechanisms. For example, exposure of many cell types (e.g., fat cells, macrophages, and endothelial cells) to saturated fatty acids such as palmitate (palm fat) activates the proinflammatory pathway. Nutrient excess can also trigger cell inflammation by raising intracellular levels of free radicals, causing cell damage. This inflammatory response, in turn, causes insulin resistance. Importantly, these inflammation-induced responses block signalling by leptin as well as by insulin.

Given the diversity of tissues affected by nutrient excess, it is perhaps unsurprising that the hypothalamus is also susceptible. Unlike inflammation in peripheral tissues, however, this hypothalamic response has the potential to cause obesity, rather than simply being its consequence. This is because leptin and insulin are crucial signals that convey “fat cell negative feedback” information to the hypothalamus regarding the amount of body fuel stored in the form of fat. When input from these hormones is reduced, therefore, the hypothalamus perceives this as evidence of reduced body fat and triggers an adaptive increase of food intake relative to energy expenditure that favours weight gain. Indeed, the same phenomenon helps to explain why it is so hard to keep off weight lost through caloric ally restricted diets. Accordingly, when inflammation-induced impairment of insulin and leptin occurs, this causes a state of positive energy balance until body fat stores, along with plasma leptin and insulin concentrations, rise sufficiently to overcome the resistance. This picture—increased plasma insulin and leptin levels, combined with the defence of an elevated level of body weight—is characteristic of common obesity.

The concept that common forms of obesity might arise from hypothalamic leptin resistance is not new, having first been reported in rodent models of diet-induced obesity (DIO) nearly a decade ago (El-Haschimi et al., 2000). But broad acceptance of acquired leptin resistance as a cause of common obesity has been hampered both by a lack of insight into how it occurs and by uncertainty about whether it is simply a consequence of obesity and not a cause. By offering an answer to the first question, the emerging role of hypothalamic inflammation is beginning to clarify the second.

The deleterious cascade of events initiated by a high fat diet are: hypothalamic inflammation, leptin resistance, obesity, and peripheral metabolic dysfunction.

References

  • De Souza et al., 2005 C.T. De Souza, E.P. Araujo, S. Bordin, R. Ashimine, R.L. Zollner, A.C. Boschero, M.J. Saad and L.A. Velloso, Endocrinology 146 (2005), pp. 4192–4199.
  • El-Haschimi et al., 2000 K. El-Haschimi, D.D. Pierroz, S.M. Hileman, C. Bjørbaek and J.S. Flier, J. Clin. Invest. 105 (2000), pp. 1827–1832.
  • Hotamisligil, 2006 G.S. Hotamisligil, Nature 444 (2006), pp. 860–867.
  • Kim et al., 2007 F. Kim, M. Pham, I. Luttrel, D.D. Bannerman, J. Tupper, J.P. Thaler, T.R. Hawn, E.W. Raines and M.W. Schwartz, Circ. Res. 100 (2007), pp. 1589–1596.
  • Kleinridders et al., 2009 A. Kleinridders, D. Schenten, C.A. Könner, B.F. Belgardt, J. Mauer, T. Okamura, F.T. Wunderlich, R. Medzhitov and J.C. Brüning, Cell Metab. 10 (2009), pp. 249–259 this issue.
  • Posey et al., 2008 K.A. Posey, D.J. Clegg, R.L. Printz, J. Byun, G.J. Morton, A. Vivekanandan-Giri, S. Pennathur, D.G. Baskin, J.W. Heinecke and S.C. Woods et al., Am. J. Physiol. Endocrinol. Metab. 296 (2008), pp. E1003–E1012.
  • Wisse et al., 2007 B.E. Wisse, F. Kim and M.W. Schwartz, Science 318 (2007), pp. 928–929.
  • Zhang et al., 2008 X. Zhang, G. Zhang, H. Zhang, M. Karin, H. Bai and D. Cai, Cell 135 (2008), pp. 61–73.