I really like and appreciate your blog post. Hi Lance — I actually do have an eBook in the works, so stay tuned for that! One of my favorite lunches: They do not create your weekly meal choices or offer any packaged snack foods, daily meal choices or daily dietary fresh food requirements. GI index is a good guide but does not answer the lack of good nutritional in foods that create major problems creating obesity and ill health amongst the majority of people I see. All meals are designed by nutritionists for proper nutrition with low calorie content.
Lean Cuisine is a line of low-fat frozen dinners designed for dieters and is available in your local grocer's frozen food section. Nutrisystem is a weight loss program that provides all your meals prepackaged through the mail. These foods are designed by a nutritionist to eliminate the need to plan your diet program.
Both Lean Cuisine and Nutrisystem provide prepackaged meals that complement a well-balanced diet and weight-loss program. All meals are designed by nutritionists for proper nutrition with low calorie content. Both meal programs provide foods that are easy to prepare and do not take a long time to cook.
Lean Cuisine foods are available in the frozen food section of the grocery store. They do not create your weekly meal choices or offer any packaged snack foods, daily meal choices or daily dietary fresh food requirements. Nutrisystem foods are ordered monthly and are delivered to your home. All meals are planned out in advance. You choose your meal options from breakfast, lunch, dinner, snacks and dessert sections on the monthly food order form, according to the Nutrisystem website.
Studies on leptin cerebrospinal fluid CSF levels provide evidence for the reduction in leptin crossing the BBB and reaching obesity-relevant targets, such as the hypothalamus, in obese people.
Since the amount and quality of leptin receptors in the hypothalamus appears to be normal in the majority of obese humans as judged from leptin-mRNA studies ,  it is likely that the leptin resistance in these individuals is due to a post leptin-receptor deficit, similar to the post-insulin receptor defect seen in type 2 diabetes. When leptin binds with the leptin receptor, it activates a number of pathways.
Mice with a mutation in the leptin receptor gene that prevents the activation of STAT3 are obese and exhibit hyperphagia. The PI3K pathway may also be involved in leptin resistance, as has been demonstrated in mice by artificial blocking of PI3K signalling. The PI3K pathway also is activated by the insulin receptor and is therefore an important area where leptin and insulin act together as part of energy homeostasis.
The consumption of a high fructose diet from birth has been associated with a reduction in leptin levels and reduced expression of leptin receptor mRNA in rats. Long-term consumption of fructose in rats has been shown to increase levels of triglycerides and trigger leptin and insulin resistance,   however, another study found that leptin resistance only developed in the presence of both high fructose and high fat levels in the diet. A third study found that high fructose levels reversed leptin resistance in rats given a high fat diet.
The contradictory results mean that it is uncertain whether leptin resistance is caused by high levels of carbohydrates or fats, or if an increase of both, is needed. Leptin is known to interact with amylin , a hormone involved in gastric emptying and creating a feeling of fullness. When both leptin and amylin were given to obese, leptin-resistant rats, sustained weight loss was seen.
Due to its apparent ability to reverse leptin resistance, amylin has been suggested as possible therapy for obesity. It has been suggested that the main role of leptin is to act as a starvation signal when levels are low, to help maintain fat stores for survival during times of starvation, rather than a satiety signal to prevent overeating.
Leptin levels signal when an animal has enough stored energy to spend it in pursuits besides acquiring food. Dieters who lose weight, particularly those with an overabundance of fat cells, experience a drop in levels of circulating leptin.
This drop causes reversible decreases in thyroid activity, sympathetic tone, and energy expenditure in skeletal muscle, and increases in muscle efficiency and parasympathetic tone. A decline in levels of circulating leptin also changes brain activity in areas involved in the regulatory, emotional, and cognitive control of appetite that are reversed by administration of leptin.
Osteoarthritis and obesity are closely linked. Obesity is one of the most important preventable factors for the development of osteoarthritis. Originally, the relationship between osteoarthritis and obesity was considered to be exclusively biomechanically based, according to which the excess weight caused the joint to become worn down more quickly. However, today we recognise that there is also a metabolic component which explains why obesity is a risk factor for osteoarthritis, not only for weight-bearing joints for example, the knees , but also for joints that do not bear weight for example, the hands.
Thus, the deregulated production of adipokines and inflammatory mediators, hyperlipidaemia, and the increase of systemic oxidative stress are conditions frequently associated with obesity which can favour joint degeneration.
Furthermore, many regulation factors have been implicated in the development, maintenance and function, both of adipose tissues, as well as of the cartilage and other joint tissues. Alterations in these factors can be the additional link between obesity and osteoarthritis. Adipocytes interact with other cells through producing and secreting a variety of signalling molecules, including the cell signalling proteins known as adipokines.
Certain adipokines can be considered as hormones, as they regulate the functions of organs at a distance, and several of them have been specifically involved in the physiopathology of joint diseases.
In particular, there is one, leptin, which has been the focus of attention for research in recent years. The circulating leptin levels are positively correlated with the Body Mass Index BMI , more specifically with fatty mass, and obese individuals have higher leptin levels in their blood circulation, compared with non-obese individuals. In addition to the function of regulating energy homeostasis, leptin carries out a role in other physiological functions such as neuroendocrine communication, reproduction, angiogenesis and bone formation.
More recently, leptin has been recognised as a cytokine factor as well as with pleiotropic actions also in the immune response and inflammation. Leptin has thus emerged as a candidate to link obesity and osteoarthritis and serves as an apparent objective as a nutritional treatment for osteoarthritis. As in the plasma, the leptin levels in the synovial fluid are positively correlated with BMI. Leptin has been shown to be produced by chondrocytes, as well as by other tissues in the joints, including the synovial tissue, osteophytes, the meniscus and bone.
The risk of suffering osteoarthritis can be decreased with weight loss. This reduction of risk is related in part with the decrease of the load on the joint, but also in the decrease of fatty mass, the central adipose tissue and the low-level inflammation associated with obesity and systemic factors.
This growing evidence points to leptin as a cartilage degradation factor in the pathogenesis of osteoarthritis, and as a potential biomarker in the progression of the disease, which suggests that leptin, as well as regulation and signalling mechanisms, can be a new and promising target in the treatment of osteoarthritis, especially in obese patients. Obese individuals are predisposed to developing osteoarthritis, not only due to the excess mechanical load, but also due to the excess expression of soluble factors, that is, leptin and pro-inflammatory cytokines, which contribute to joint inflammation and cartilage destruction.
As such, obese individuals are in an altered state, due to a metabolic insufficiency, which requires specific nutritional treatment capable of normalising the leptin production and reducing the systematic low-level inflammation, in order to reduce the harmful impact of these systematic mediators on the joint health. There are nutritional supplements and pharmacological agents capable of directing these factors and improving both conditions.
Leptin was approved in the United States in for use in congenital leptin deficiency and generalized lipodystrophy. An analog of human leptin metreleptin trade name Myalept was first approved in Japan in , and in the United States in February In the US it is indicated as a treatment for complications of leptin deficiency, and for the diabetes and hypertriglyceridemia associated with congenital or acquired generalized lipodystrophy.
From Wikipedia, the free encyclopedia. Not to be confused with Lectin or Lecithin. Structure of the obese protein leptin-E Leptin plays a critical role in the adaptive response to starvation. Leptin receptor and Energy expenditure. Bearing in mind that other hormones such as ghrelin operate in a faster-time scale, it would be misleading to define it as "the satiety hormone". Nat Clin Pract Endocrinol Metab. World Rev Nutr Diet. Crit Rev Food Sci Nutr. Journal of Clinical Investigation.
A complex hub among inflammation, metabolism, and immunity". The Inside Story of the Obesity Industry. RNA expression pattern and mapping on the physical, cytogenetic, and genetic maps of chromosome 7".
Wei Sheng Yan Jiu in Chinese. Studies in lean and obese subjects and during short-term fasting". Int J Sports Med. Studies in vivo and in vitro". Journal of Cellular Biochemistry. Lay summary — medicinenet. The Journal of Neuroscience. International journal of obesity Lond. Lay summary — WebMD. Arterioscler Thromb Vasc Biol. There are 5 grams of total fat, 2 grams are saturated fat. The cholesterol content is 25 mg, sodium is mg and mg of potassium. There are 29 grams of total carbohydrate, 4 grams of dietary fiber and 16 grams of protein.
The ingredients are cooked whole-grain pasta, chicken tenderloins, water, broccoli, red pepper, cornstarch, butter, Romano cheese, sea salt, garlic puree, spices and garlic powder. Per serving there are calories, 40 calories from fat.
The amount of total fat is 4. There are 25 mg of cholesterol, mg of sodium and mg of potassium. The total carbohydrate amount is 29 grams with 5 grams of dietary fiber and 5 grams of sugar. The protein content is 19 grams. The ingredient list is blanched whole-wheat vermicelli, cooked white meat chicken, skim milk, asparagus, broccoli, tomatoes, and 2 percent or less of sea salt, enzyme modified Parmesan cheese, Asiago cheese, Parmesan cheese, salt, roasted garlic, modified cornstarch, soybean oil, bleached wheat flour, basil, garlic puree, sugar, autolyzed yeast extract, seasoning, potassium chloride, whey, lactic acid, calcium lactate and spice.
Per serving there are calories, 35 calories from fat. The total fat content is 4 grams, 2 grams of saturated fat. There are 5 mg of cholesterol and mg of sodium. Potassium is not listed.