Obesity Management In Asthama

Asthma is a chronic disorder affecting millions of people worldwide. The prevalence of asthma is around 300 million and is expected to increase another 100 million by 2025. Obesity, on the other hand, also affects a large number of individuals. Overweight in adults is defined when body mass index (BMI) is between 25 to 30 kg/m2 and obesity when the BMI >30 kg/m2. It has been a matter of interest for researchers to find a relation between these two conditions. This knowledge will provide a new insight into the management of both conditions. At present, obese asthma patients may be considered a special category and it is important to assess the impact of management of obesity on asthma symptoms.

KEY WORDS: Asthma, body mass index, obesity.

EFFECT OF OBESITY
Physiological consequences

Obesity usually causes a restrictive effect on the lungs. Ricard et al. (2006) has shown that there is a linear relation of decreased lung volumes and BMI.[27] At a BMI of 30 kg/m2, functional residual capacity (FRC) was reduced to 75% and expiratory reserve volume (ERV) reduced to 40% that of a lean individual with a BMI of 20 kg/m2. More reduction in lung volumes was seen in overweight and mildly obese individuals. There is a moderate reduction in total lung capacity (TLC) and greater reduction of functional residual capacity (FRC).[19] A majority of the morbid obese individuals breathe around the closing volume.[28,29] Moreover, Fredberg et al. (1997) and other similar studies showed that decrease in FRC and tidal volumes leads to small cycling rates, leading to the conversion of airway smooth muscle from rapid cycle actin-myosin cross bridges to slow cycle latch bridges.  The attainment of the latch state in obese asthmatics, due to an increased frequency of detachment rate of actin-myocin may be considered a reason for persistent obstruction in asthmatic airways.  Increased airway responsiveness has been found to be associated with the latch state of airway smooth muscles.[30–32] Moreover, breathing around the closing volume may enhance these effects.[32–35] Some studies have shown a decrease in the forced expiratory flow in the mid portion of FVC (FEF25-75) in obese individuals.  Litonjua et al., (1999) in their study, found that t he FEF25-75/FVC ratio is independently associated with increase methacholine responsiveness of the airways.  Reduction in lung volumes is proportionate to the degree of obesity. Moreover, these physiological changes can be reversed on reduction of weight.  Respiratory resistance increases in obese individuals, but when airway resistance is calculated by adjusting for lung volumes, it was found to be within normal limits.  It is possible that other mechanisms, apart from mechanical effect, may lead to increased airway resistance, like airway remodeling, peripheral airway obstruction etc.  This hypothesis needs further studies for confirmation. Therefore, obesity did not cause obstruction of airways and moreover, FEV1 to FVC ratio remained either normal or increased.[19] Wang and his colleagues (2006) have shown increased airway hyper responsiveness with increase BMI.[41] However, Nicolacakis et al. (2008) showed that obesity per se does not alter bronchial reactivity.  This study stated that obesity and asthma independently affect the function of the lungs.

Moreover, there is reduction of respiratory system compliance.  This may be due to excess soft tissue weight compressing the thoracic cage, fatty infiltration of the chest wall, and an increase in pulmonary blood volume in obese individuals.  Cournand et al. (1954) shown that there is increased oxygen cost of breathing with decreased lung compliance. Sin et al. (2002) found that increase in obesity is a subjective perception of dyspnea.[49] Therefore, obesity causes a reduction in respiratory system compliance and lung volumes, leading to alteration in pulmonary blood volume, and a ventilation–perfusion mismatch.

Inflammatory consequences

In obese individuals, adepocytes act as an active endocrine organ, with increased inflammatory activity. Moreover, adepocytes may recruit other inflammatory cells and augment inflammatory responses.

Both asthma and obesity are associated with an inflammatory state. Along with increased inflammatory cells, there is also an increase in inflammatory mediators in obese individuals. Several inflammatory mediators like TNF-α, interleukin-6, interleukin 18, CRP etc., have been found to be increased.[19] Mohamed-Ali et al. (1997) has shown that IL-6 and TNFα were constitutively expressed by adipocytes.[50] Tsigos et al. (1999) showed that increased levels of IL6 and TNFα could be correlated with total fat mass, especially abdominal obesity.[51] Espostio et al. (2003), in their study have shown that medical weight loss in obese women resulted in a decrease of IL-6, IL-18 and CRP levels to a significant extent.  Striz et al. (1999) showed that TNF-α increases IL-4 mRNA production while IL-4 subsequently decreases TNF-α production.  Similarly, Salvi et al. (1999) found that TNF-α also increases production of IL-5 by bronchial epithelial cells.  Gosset et al. (1992) and Yokoyama et al. (1995), in their separate studies, showed that IL-6 production increased in asthma and has been related to stimulation with histamine, IL-4, TNF- α, and IL-1.[55,56] It has been found that IL-6 may be responsible for the IL-4 mediated IgE production.  However, these markers are more closely related to central obesity. Thuesen et al. has shown that insulin resistance in centrally obese patients is more closely related to asthma like symptoms than obesity or BMI itself. 

Hormones

Obesity results in changes in the level of energy regulating hormones from adepocytes. Leptin and adiponectin are two hormones of this type released by adepocytes. 

Leptin, also known as the satiety hormone works as a proinflammatory mediator.[19] Leptin is coded by the Ob gene. Sierra-Honigmann and collegues (1998) showed that leptin shares a structural similarity with long-chain helical cytokines, like IL-6, and has been found to be associated with proliferation and activation of T-cells, recruitment and activation of monocytes and macrophages, and promotes angiogenesis.[59] Shore et al. (2005) sensitized and challenged lean BALB/cJ mice with ovalbumin and then infused either saline or leptin subcutaneously. They found that after leptin infusion, serum leptin levels increased, with associated enhancement of airway hyperresponsiveness (AHR), and an increase in serum IgE following inhaled ovalbumin challenge. However, these changes were not observed with saline infusion.  Similar studies in animals have also shown that leptin treatment leads to increase in allergen induced airway hyperresponsivness. However, there is no increase in eosinophil influx or Th2 cytokine expression.  This suggests that leptin works through a mechanism that is independent of Th2 response. Studies have also shown increased levels of leptin in patients with asthma. However, certain studies showed that leptin has a significant immunomodulatory role, irrespective of body mass. 

Adiponectin is an insulin sensitizing hormone released by adipocytes. It has anti-inflammatory effects and its levels decrease in obese individuals.  Adiponectin acts on macrophages and monocytes to inhibit production of proinflammatory cytokines and to augment IL-10 and IL-1 receptor antagonist expression.  Shore et al. (2006) in their animal study in mice showed that exogenous administration of adiponectin results in an almost complete suppression of allergen-induced AHR, airway inflammation, and Th2 cytokine expression.[65] Decline in the mRNA expression of all 3 adeponectin receptors in the lungs, after allergen sensitization and challenge in mice, suggests that asthma may be a adiponectin resistance state.[65] Kadowaki et al. (2008) and similar studies showed obesity-related decline in adiponectin.  Shore et al. (2006) showed additional decline in serum adiponectin with allergen challenge.  Therefore, obese patients with asthma may have defects in this important immunomodulatory pathway that augments the effects of an allergen challenge. 

Some studies have shown an increased association of obesity with asthma among women, compared to men. This may be due to hormonal differences, mostly attributable to the sex hormone estrogen. Troisi et al., in their study of the relation between menopause, postmenopausal hormone replacement therapy (HRT) and asthma has shown significantly increased relative risk of incident asthma in women on HRT (RR 1.49). Moreover, studies have shown that estrogen increases IL-4 and IL-13 production and increases eosinophil recruitment and degranulation,  which are also observed in asthma patients.

Co-morbidities

Several co-morbidities have been associated with obesity and it is supposed to be a contributing factor in asthma symptoms.

Obesity is commonly associated with dyslipedemia. Animal studies  have shown that a high-cholesterol diet promotes Th2 inflammation in mouse models of asthma. However, this can be reversed by a lipid lowering agent.  Al-Shawwa and collegues (2006), in their study, showed a higher prevalence of asthma in children with high serum cholesterol.  However, the study population was small and the results need further confirmation.

GERD and sleep disordered breathing (SDB) are also important co-morbid conditions in obesity. GERD and SDB are thought to increase the risk for asthma. Gunnbjornsdottir et al. (2004) and Sluit et al. (2005), in separate studies, showed that habitual snoring, or SDB did not substantially affect the relationship between obesity and asthma, when adjusted for GERD.[74,75] Therefore, an increased risk of asthma in the obese may be independent of GERD and SDB. When a person adopts the supine posture, there is further reduction of FRC in the obese which may thus exacerbate asthma symptoms. Moreover, continuous positive airway pressure, a treatment used extensively in the treatment of SDB, elevates the FRC, improving the quality of life in an asthma patient.More studies are required in this context to confirm or refute this relation.

Al-Shawwa and colleagues (2007) reported a higher prevalence of insulin resistance among obese children with asthma, compared with obese children without asthma. The study included a small number of subjects and needs further confirmation. Moreover, studies have shown that only the subset of obese individuals with central adiposity and insulin resistance demonstrated enhanced systemic inflammation.Thuesen et al. (2009) showed that insulin resistance was associated with incident wheezing (OR 1.87, 95% CI 1.38-2.54) and asthma-like symptoms (OR 1.61, 95% CI 1.23-2.10), and was a stronger risk factor for asthma than obesity.

AFTER TRANSFORMATION

Obesity Management In Varicose Veins

We all know that being overweight can lead to various health problems. Some of these, such as diabetes and premature arthritis make the news every day. What is not highlighted in the press much is that obesity can also ‘hide’ certain common conditions, such as varicose veins.

About 30% of people develop varicose veins at some point in their lives and some of them will be overweight. For people of a normal body size, the vein problem is usually obvious, because bulging veins are visible on the skin of the calf. The leaking veins also cause discomfort and heaviness of the legs - these symptoms in overweight patients are often attributed to the weight problem itself rather than the possibility of a varicose vein.

As I have noticed over the years at my clinic, obese people sometimes don’t realise that they have varicose veins, as the swollen veins are not visible on the surface of the skin, due to the excess fat - in other words, the problem is hidden from view. Over time, the pressure in the leaking veins can cause damage to the skin on the lower leg. Only then the patients will go and see a specialist. This is a major problem in the overweight population, who are at greater risk of leg ulceration.

For overweight people, varicose veins are also more difficult to assess and treat. Vein issues are usually diagnosed by a duplex ultrasound scan - this non-invasive investigation can ‘see’ under the skin and locate the faulty vein. The technician then produces a ‘vein map’ of where the problems are in the vein system, which the surgeon can then use to direct the treatment to the right place. These veins in a standard size leg are usually 1 or 2 cm under the skin. In very large legs, the scanning is much more difficult to do as the veins are often 4 or 5 cm inside the leg, so much harder to detect accurately.

In addition, the depth of the veins in the leg makes it more difficult for the surgeon to treat the problem. The minimally invasive options of laser treatment are much more challenging in larger legs and much more uncomfortable for the patient if they are choosing the local anaesthetic option. On the other hand, giving overweight patients a general anaesthetic carries more risk than for someone of a normal body size. Finally, the option of the somewhat out of favour ‘high tie and strip’ operation is also unpalatable as an incision in the groin crease in overweight patients carries a high risk of wound infection.

For patients not fit enough or unsuitable for varicose vein surgery the alternative non-surgical solution of compression stockings is also more difficult. Compression stockings are notoriously prone to slipping down the leg. This is more frequent in certain leg shapes, especially where the thigh is very large. Stockings that slip down and bunch up tightly behind the knee can make veins worse rather than better.

Being overweight can therefore cause issues in diagnosing and treating certain conditions, as well as living with them. This should definitely be one more good reason to maintain or aim for a healthy weight and tackle the obesity epidemic.

AFTER TRANSFORMATION

Obesity Management In Osteoarthritis

“We know that obesity is the number-one preventable risk factor for osteoarthritis but it hasn’t been studied much because everyone dismissed it as overloading joints,”

He and others began to wonder whether obesity alone told the whole story of joint destruction. Some athletic endeavors put greater biomechanical forces on knees than obesity. And, people who are obese are more likely to have osteoarthritis (OA) in their wrists, fingers and hands. Our hands sometimes bear loads (think of carrying a heavy flower pot) but not our body weight (we don’t walk on our hands).

  overweight as to be deemed obese (defined as twenty pounds heavier than your upper weight range), those excess pounds of fat carry hidden dangers.

Fat, or adipose tissue in medical lingo, is home to millions upon millions of busy adipocytes, or fat cells. A flurry of research over the past few years is starting to explain how adipocytes work against the body to destroy joints by misguided responses to high levels of glucose and exposure to cytokines (immune proteins). In reaction to such exposure, adipocytes churn out high levels of their own immune proteins called adipokines.

Year after year of obesity fuels a steady barrage of friendly fire that in turn generates low-level chronic inflammation. Not an inflamed immune system, like an infection but a soft drum-beat of immune proteins that over time can damage tissues such as joints,

To study the link between a disrupted metabolic system and osteoarthritis,   In work recently published in Arthritis Research and Therapy, Mooney’s team studied whether a high-fat diet in diabetic mice would damage joints.

One group of mice ate a high-fat diet and then had surgery that mimics knee injuries in people and is designed to quickly bring on osteoarthritis. The second group of mice ate regular mouse chow until they had the surgery, and then ate the high-fat diet after surgery. At monthly intervals, the team examined bone and cartilage tissues in the knee joints for markers that would reveal signs of osteoarthritis.

The mice fed the high-fat diet before and after surgery ended up with a body weight considered obese; mice fed the high-fat diet after surgery gained more weight than controls but were not obese.

  with abnormal changes to their metabolism and early signs of OA. As it turns out, obesity alone wasn’t enough to damage joints; even mice that weighed less had changes in their joint tissue that showed the progression to OA. In all mice, such metabolic disturbances occurred long before mice gained a lot of weight.

 “These results argue that all you need is metabolic changes. You don’t need gross weight gain to have changes in the progression of osteoarthritis,” says Mooney. 

Next Mooney’s team will try and decipher the molecular pathways that lead from metabolic disturbances to joint damage. Mooney will also use his expertise in diabetes to see whether insulin resistance – a condition in which the tissues don’t respond to insulin well and thus can’t lower blood sugar – plays a role in damaging joints. These efforts may bring to light a potential therapy; perhaps correcting diabetes and correct insulin resistance will slow down progression to OA,  

The link between obesity and OA is actually very complicated. Adipocytes secrete many adipokines, one of which includes leptin, which regulates metabolism and body weight. Researchers need to figure out whether leptin and its protein cousins can damage cartilage directly or whether they recruit other cells for their dirty work.   they discovered that many are exactly the same immune proteins that OA researchers have been studying for years, “and no one had put them together to say all of the stuff in your joints may be coming from the fat,

As it happens, mice love to run, so the team gave some of the mice on the high-fat diet access to a running wheel; the other mice on the high fat diet didn’t run at all. All of the mice ended up obese, even mice that ran the equivalent of two miles each night. But tests on the mice that were allowed exercise showed that exercise alone slowed down the immune proteins that lead to inflammation, and reduced the severity of OA.

AFTER TRANSFORMATION

Obesity Management On Slip Disc

A 'slipped' (prolapsed) disc often causes severe lower back pain. The disc often presses on a nerve root which can cause pain and other symptoms in a leg. In most cases, the symptoms ease off gradually over several weeks. The usual advice is to do normal activities as much as possible. Painkillers may help. Physical treatments such as spinal manipulation may also help. Surgery may be an option if the symptoms persist.

Understanding the back

The spine is made up of many bones called vertebrae. These are roughly circular and between each vertebra is a disc. The discs are made of strong rubber-like tissue which allows the spine to be fairly flexible. A disc has a stronger fibrous outer part and a softer jelly-like middle part called the nucleus pulposus.

The spinal cord, which contains the nerves that come from the brain, is protected by the spine. Nerves from the spinal cord come out from between the vertebrae to relay messages to and from various parts of the body.

Strong ligaments attach to the vertebrae. These give extra support and strength to the spine. Various muscles also surround, and are attached to, various parts of the spine. (The muscles and ligaments are not shown in the diagram below, for clarity.)

Note: this leaflet is about a 'slipped' (prolapsed) disc in the lower back (the lumbar spine). There is a separate leaflet about disc problems in the neck, called Cervical Spondylosis.

What is a prolapsed disc?

Prolapsed disc

When you have a 'slipped' (prolapsed) disc, a disc does not actually slip. What happens is that part of the inner softer part of the disc (the nucleus pulposus) bulges out (herniates) through a weakness in the outer part of the disc. A prolapsed disc is sometimes called a herniated disc. The bulging disc may press on nearby structures such as a nerve coming from the spinal cord. Some inflammation also develops around the prolapsed part of the disc.

Any disc in the spine can prolapse. However, most prolapsed discs occur in the lower back (the lumbar spine). The size of the prolapse can vary. As a rule, the larger the prolapse, the more severe the symptoms are likely to be.

Who gets a prolapsed disc?

Bouts of back pain are very common. However, less than 1 in 20 cases of sudden-onset (acute) back pain are due to a 'slipped' (prolapsed) disc. (Most cases of back pain are classed as simple low back pain. This is thought to be caused by a minor problem in a muscle, ligament, or other structure in the back - for example, a strained muscle. See separate leaflet called Nonspecific Lower Back Pain in Adults for a general overview of the different types of back pain.)

The most common age to develop a prolapsed disc is between 30 and 50 years. Twice as many men as women are affected.

What causes a prolapsed disc?

It is not clear why some people develop a 'slipped' (prolapsed) disc and not others, even when they do the same job or lift the same sort of objects. It seems that some people may have a weakness in the outer part of the affected disc. Various things may trigger the inner softer part of the disc to prolapse out through the weakened outer part of the disc. For example, sneezing, awkward bending, or heavy lifting in an awkward position may cause some extra pressure on the disc. In people with a weakness in a disc, this may be sufficient to cause a prolapse. Factors that may increase the risk of developing a prolapsed disc include:

A job involving lots of lifting.

A job involving lots of sitting (especially driving).

Weight-bearing sports (weightlifting, etc).

Smoking.

Being overweight (obesity).

Increasing age (a disc is more likely to develop a weakness with increasing age).

What are the symptoms of a prolapsed disc?

Back pain

The pain is often severe and usually comes on suddenly. The pain is usually eased by lying down flat and is often made worse if you move your back, cough or sneeze.

Nerve root pain (usually sciatica)

Nerve root pain is pain that occurs because a nerve coming from the spinal cord is pressed on (trapped) by a 'slipped' (prolapsed) disc, or is irritated by the inflammation caused by the prolapsed disc. Although the problem is in the back, you feel pain along the course of the nerve in addition to back pain. Therefore, you may feel pain down a leg to the calf or foot. Nerve root pain can range from mild to severe but it is often worse than the back pain. With a prolapsed disc, the sciatic nerve is the most commonly affected nerve. (The term sciatica means nerve root pain of the sciatic nerve.) The sciatic nerve is a large nerve that is made up from several smaller nerves that come out from the spinal cord in the lower back. It travels deep inside the buttock and down the back of the leg. There is a sciatic nerve for each leg.

Other nerve root symptoms

The irritation or pressure on the nerve next to the spine may also cause pins and needles, numbness or weakness in part of a buttock, leg or foot. The exact site and type of symptoms depend on which nerve is affected.

Related discussions

Sineadsmith90

New burning sensation in leg/foot

Sineadsmith90

0replies

Gaz88

Herniated disc - sciatica

Gaz88

0replies

julie93078

Post microdiscectomy surgery muscle spasms

julie93078

3replies

Start a discussion

Cauda equina syndrome - rare, but an emergency

Cauda equina syndrome is a particularly serious type of nerve root problem that can be caused by a prolapsed disc. This is a rare disorder where the nerves at the very bottom of the spinal cord are pressed on. This syndrome can cause low back pain plus:

Problems with bowel and bladder function (usually inability to pass urine).

Numbness in the saddle area around the back passage (anus).

Weakness in one or both legs.

This syndrome needs urgent treatment to preserve the nerves to the bladder and bowel from becoming permanently damaged. See a doctor immediately if you develop these symptoms.

Some people do not have symptoms

Research studies where routine back scans have been done on a large number of people have shown that some people have a prolapsed disc without any symptoms. It is thought that symptoms mainly occur if the prolapse causes pressure on or irritation of a nerve. This does not happen in all cases. Some prolapses may be small, or occur away from the nerves and cause minor or no symptoms.

How does a prolapsed disc progress?

In most cases, the symptoms tend to improve over a few weeks. Research studies of repeated MRI scans have shown that the bulging prolapsed portion of the disc tends to get smaller (regress) over time in most cases. The symptoms then tend to ease and, in may cases, go. In only about 1 in 10 cases is the pain still bad enough after six weeks to consider surgery (see below).

Do I need any tests?

Your doctor will normally be able to diagnose a 'slipped' (prolapsed) disc from the symptoms and by examining you. (It is the common cause of sudden back pain with nerve root symptoms.) In most cases, no tests are needed, as the symptoms often settle within a few weeks.

Tests such as X-rays or scans may be advised if symptoms persist. In particular, an MRI scan can show the site and size of a prolapsed disc. This information is needed if treatment with surgery is being considered.

What are the treatments for a prolapsed disc?

Exercise and keep going

Continue with normal activities as far as possible. This may not be possible at first if the pain is very bad. However, move around as soon as possible and get back into normal activities as soon as you are able. As a rule, don't do anything that causes a lot of pain. However, you will have to accept some discomfort when you are trying to keep active. Setting a new goal each day may be a good idea - for example, walking around the house on one day, a walk to the shops the next, etc.

In the past, advice had been to rest until the pain eases. It is now known that this was wrong. You are likely to recover more quickly and are less likely to develop persistent (chronic) back pain if you keep active when you have back pain rather than rest a lot. Also, sleep in the most naturally comfortable position on whatever is the most comfortable surface. (Advice given in the past used to be to sleep on a firm mattress. However, there is no evidence to say that a firm mattress is better than any other type of mattress for people with back pain.)

Medication

If you need painkillers, it is best to take them regularly. This is better than taking them now and again just when the pain is very bad. If you take them regularly the pain is more likely to be eased for much of the time, enabling you to exercise and keep active.

Paracetamol is often sufficient if you take it regularly at full strength. For an adult, this is 1000 mg (usually two 500 mg tablets), four times a day.

Anti-inflammatory painkillers. Some people find that these work better than paracetamol. They include ibuprofen which you can buy at pharmacies or obtain on prescription. Other types such as diclofenac or naproxen need a prescription. Some people with asthma, high blood pressure, kidney failure, or heart failure may not be able to take anti-inflammatories.

A stronger painkiller such as codeine is an option if anti-inflammatories do not suit or do not work well. Codeine is often taken in addition to paracetamol. Constipation is a common side-effect from codeine. This may make back pain worse if you need to strain to go to the toilet. To prevent constipation, have lots to drink and eat foods with plenty of fibre.

A muscle relaxant such as diazepam is sometimes prescribed for a few days if the back muscles become very tense and make the pain worse.

Physical treatments

Some people visit a physiotherapist, chiropractor or osteopath for manipulation and/or other physical treatments. It is debatable whether physical treatments would help all people with a 'slipped' (prolapsed) disc. However, physical treatments provide some short-term comfort and hasten recovery in some cases.

Surgery

Surgery may be an option in some cases. As a rule, surgery may be considered if the symptoms have not settled after about six weeks or so. This is the minority of cases as, in about 9 in 10 cases, the symptoms have eased off and are not bad enough to warrant surgery within about six weeks.

The aim of surgery is to cut out the prolapsed part of the disc. This often eases symptoms. However, it does not work in every case. Also, as with all operations, there is a risk from surgery. A specialist will advise on the pros and cons of surgery and on the different techniques that are available.

Can further bouts of back pain and/or prolapsed disc be prevented?

Evidence suggests that the best way to prevent bouts of back pain and 'slipped' (prolapsed) disc is simply to keep active and to exercise regularly. This means general fitness exercise such as walking, running, swimming, etc. There is no firm evidence to say that any particular back strengthening exercises are more useful than simply keeping fit and active. It is also sensible to be back-aware. For example, do not lift objects when you are in an awkward twisting posture.

Fatty Liver And Obesity Management

Obesity is defined as an excess amount of body fat. The normal amount of body fat (expressed as a percentage of body weight) is between 25-30% in women and 18-23% in men. Women with over 30% body fat and men with over 25% body fat are considered obese. Another easier way of defining obesity is by calculating the body mass index (BMI). The BMI is a mathematical formula that takes into account both a person's weight and height in calculating the degree of obesity. In adults, normal weight is defined as a BMI between 20 and 25 BMI units, overweight from 25 to 30, obesity from 30 to 35, significant obesity from 35 to 40, morbid obesity from 40 to 45, super obesity from 45 to 50, and super-morbid obesity greater than 50. Eighty percent of deaths related to obesity occurs in obese individuals with a BMI greater than 30. To find out what your BMI is, please refer to the Body Mass Index (BMI) Table for Adults, and the Body Mass Index (BMI) Index Table for Teens.

What is nonalcoholic fatty liver disease (NAFLD)?

Nonalcoholic fatty liver disease (NAFLD) refers to a wide spectrum of liver diseases ranging from the most common, fatty liver (accumulation of fat in the liver, also known as steatosis), to Nonalcoholic steatohepatitis (NASH, fat in the liver causing liver inflammation), to cirrhosis (irreversible, advanced scarring of the liver as a result of chronic inflammation of the liver). All of the stages of Nonalcoholic fatty liver disease are now believed to be due to insulin resistance, a condition closely associated with obesity. In fact, the BMI correlates with the degree of liver damage, that is, the greater the BMI the greater the liver damage.

The term Nonalcoholic is used because liver disease due to alcohol can show the same spectrum of liver disease as nonalcoholic fatty liver disease; however, patients with nonalcoholic fatty liver disease do not consume excessive amounts of alcohol.

In most patients nonalcoholic fatty liver disease causes no symptoms. Nonalcoholic fatty liver disease often is discovered when routine blood tests show slightly elevated levels of liver enzymes (ALT and AST) in the blood. Another way in which nonalcoholic fatty liver disease is discovered is whenultrasound examination of the abdomen is done for other purposes, say for looking for gallstones, and fat is found in the liver. In the late stages of non alcoholic fatty liver disease, the development of cirrhosis can lead to failure of the liver, swelling of the legs (edema, accumulation of fluid in the abdomen (ascites), bleeding from veins in the esophagus (varices), and mental confusioN (hepatic encephalopath Patients with cirrhosis caused by Nonalcoholic fatty liver disease also may be at risk of developingliver cancer (hepatocellular carcinoma HCC).

One common cause of liver failure (and thus a common reason for transplantation of the liver) is cryptogenic cirrhosis (cryptogenic meaning that the cause of the cirrhosis is unknown). Doctors now believe that a large number of patients with cryptogenic cirrhosis are actually patients in the late stages of nonalcoholic fatty liver disease. Doctors and public health officials project that obesity related liver diseases (cryptogenic cirrhosis and liver cancer) will become the leading cause of liver failure and liver transplantation in the not too distant future.

How are nonalcoholic fatty liver disease and nonalcoholic steatohepatitis treated? 

Losing excess weight is the cornerstone of treatment of nonalcoholic fatty liver disease. One retrospective study (that is, a study that looks back in time) found that among obese individuals with elevated transaminases, weight gain led to a further increase in the level of the liver enzymes. In contrast, a 10% loss of weight leads to a significant decrease in the levels of the enzymes, and the enzymes even may become normal. The decrease in enzymes occurred at the rate of 8% per 1% loss of body weight. In studies of patients undergoing stomach (gastric) reduction operations for morbid obesity, substantial weight loss is accompanied by a marked reduction in transaminases and a regression (improvement) of non alcoholic fatty liver disease.

Doctors also are using medications to treat nonalcoholic fatty liver disease. For example, insulin-sensitizing agents, such as the thiazolidinediones, pioglitazone (Actos) and rosiglitazone (Avandia), and metformin (Glucophage) not only help to control blood glucose in patients with diabetes, but they also improve enzyme levels in patients with Nonalcoholic fatty liver disease. Medications in the statin class of drugs (for example, atorvastatin/Lipitor) decrease the bad LDL cholesterol and, improve enzyme levels among patients with atorvastatin. More studies are necessary to determine whether these medications also reduce the amount of fat and inflammation in the liver.

Early uncontrolled studies (not the strongest type of studies) suggested possible benefit of ursodiol (Actigall, Urso) and vitamin E in treating atorvastatin, but more recent studies showed no benefit of either of these medications in treating atorvastatin.

The bottom line, however, is that the single most effective treatment for obese people with Nonalcoholic steatohepatitis is to simply lose weight through diet and exercise. Unfortunately, this is no easy task in a society dominated by a sedentary lifestyle and high-calorie, high-carbohydrate, high-fat diets. With great effort, however, weight loss is achievable. Furthermore, in view of the possible detrimental effects of fat in other liver diseases, weight loss might be added to the treatment of other liver diseases that are not primarily due to fat, such as hepatitis C. Ultimately, non alcoholic steatohepatitis probably can be largely prevented and eliminated by promoting healthy eating habits and active lifestyles in children, where it all begins.

BEFORE TRANSFORMATION

AFTER TRANSFORMATION

Obesity Management In Breast Cancer

What is known about the relationship between obesity and cancer?

Obesity is associated with increased risks of the following cancer types, and possibly others as well:

Esophagus

Pancreas

Colon and rectum

Breast (after menopause)

Endometrium (lining of the uterus)

Kidney

Thyroid

Gallbladder

One study, using NCI Surveillance, Epidemiology, and End Results (SEER) data, estimated that in 2007 in the United States, about 34,000 new cases of cancer in men (4 percent) and 50,500 in women (7 percent) were due to obesity. The percentage of cases attributed to obesity varied widely for different cancer types but was as high as 40 percent for some cancers, particularly endometrial cancer and esophageal adenocarcinoma.

A projection of the future health and economic burden of obesity in 2030 estimated that continuation of existing trends in obesity will lead to about 500,000 additional cases of cancer in the United States by 2030. This analysis also found that if every adult reduced their BMI by 1 percent, which would be equivalent to a weight loss of roughly 1 kg (or 2.2 lbs) for an adult of average weight, this would prevent the increase in the number of cancer cases and actually result in the avoidance of about 100,000 new cases of cancer.

Several possible mechanisms have been suggested to explain the association of obesity with increased risk of certain cancers:

Fat tissue produces excess amounts of estrogen, high levels of which have been associated with the risk of breast, endometrial, and some other cancers.

Obese people often have increased levels of insulin and insulin-like growth factor-1 (IGF-1) in their blood (a condition known as hyperinsulinemia or insulin resistance), which may promote the development of certain tumors.

Fat cells produce hormones, called adipokines, that may stimulate or inhibit cell growth. For example, leptin, which is more abundant in obese people, seems to promote cell proliferation, whereas adiponectin, which is less abundant in obese people, may have antiproliferative effects.

Fat cells may also have direct and indirect effects on other tumor growth regulators, including mammalian target of rapamycin (mTOR) and AMP-activated protein kinase.

Obese people often have chronic low-level, or “subacute,” inflammation, which has been associated with increased cancer risk.

Other possible mechanisms include altered immune responses, effects on the nuclear factor kappa beta system, and oxidative stress.

What is known about the relationship between obesity and breast cancer?

Many studies have shown that overweight and obesity are associated with a modest increase in risk of postmenopausal breast cancer. This higher risk is seen mainly in women who have never used menopausal hormone therapy (MHT) and for tumors that express both estrogen and progesterone receptors.

Overweight and obesity have, by contrast, been found to be associated with a reduced risk of premenopausal breast cancer in some studies.

The relationship between obesity and breast cancer may be affected by the stage of life in which a woman gains weight and becomes obese. Epidemiologists are actively working to address this question. Weight gain during adult life, most often from about age 18 to between the ages of 50 and 60, has been consistently associated with risk of breast cancer after menopause.

The increased risk of postmenopausal breast cancer is thought to be due to increased levels of estrogen in obese women. After menopause, when the ovaries stop producing hormones, fat tissue becomes the most important source of estrogen. Because obese women have more fat tissue, their estrogen levels are higher, potentially leading to more rapid growth of estrogen-responsive breast tumors.

The relationship between obesity and breast cancer risk may also vary by race and ethnicity. There is limited evidence that the risk associated with overweight and obesity may be less among African American and Hispanic women than among white women.

What is known about the relationship between obesity and endometrial cancer?

Overweight and obesity have been consistently associated with endometrial cancer, which is cancer of the lining of the uterus. Obese and overweight women have two to four times the risk of developing this disease than women of a normal weight, regardless of menopausal status. Many studies have also found that the risk of endometrial cancer increases with increasing weight gain in adulthood, particularly among women who have never used MHT.

Although it has not yet been determined why obesity is a risk factor for endometrial cancer, some evidence points to a role for diabetes, possibly in combination with low levels of physical activity. High levels of estrogen produced by fat tissue are also likely to play a role.

What is known about the relationship between obesity and colorectal cancer?

Among men, a higher BMI is strongly associated with increased risk of colorectal cancer. The distribution of body fat appears to be an important factor, with abdominal obesity, which can be measured by waist circumference, showing the strongest association with colon cancer risk.

An association between BMI and waist circumference with colon cancer risk is also seen in women, but it is weaker. Use of MHT may modify the association in postmenopausal women.

A number of mechanisms have been proposed to account for the association of obesity with increased colon cancer risk. One hypothesis is that high levels of insulin or insulin-related growth factors in obese people may promote colon cancer development.

High BMI is also associated with rectal cancer risk, but the increase in risk is more modest.

What is known about the relationship between obesity and kidney cancer?

Obesity has been consistently associated with renal cell cancer, which is the most common form of kidney cancer, in both men and women. The mechanisms by which obesity may increase renal cell cancer risk are not well understood. High blood pressure is a known risk factor for renal cell cancer, but the relationship between obesity and kidney cancer is independent of blood pressure status. High levels of insulin may play a role in the development of the disease.

What is known about the relationship between obesity and esophageal cancer?

Overweight and obese people are about twice as likely as people of healthy weight to develop a type of esophageal cancer called esophageal adenocarcinoma. Most studies have observed no increased risk, or even a decline in risk, with obesity for the other major type of esophageal cancer, squamous cell cancer.

The mechanisms by which obesity may increase risk of esophageal adenocarcinoma are not well understood. However, overweight and obese people are more likely than people of normal weight to have a history of gastroesophageal reflux disease or Barrett esophagus, which are associated with an increased risk of esophageal adenocarcinoma. It is possible that obesity exacerbates the esophageal inflammation that is associated with these conditions.

What is known about the relationship between obesity and pancreatic cancer?

Many studies have reported a slight increase in risk of pancreatic cancer among overweight and obese individuals. Waist circumference may be a particularly important factor in the association of overweight and obesity with pancreatic cancer.

What is known about the relationship between obesity and thyroid cancer?

Increasing weight has been found to be associated with an increase in the risk of thyroid cancer. It is unclear what the mechanism might be.

What is known about the relationship between obesity and gallbladder cancer?

The risk of gallbladder cancer increases with increasing BMI. The increase in risk may be due to the higher frequency of gallstones, a strong risk factor for gallbladder cancer, in obese individuals.

What is known about the relationship between obesity and other cancers?

The relationship between obesity and prostate cancer has been studied extensively. The results of individual studies do not suggest a consistent association between obesity and prostate cancer. However, when the data from multiple studies are pooled, analyses show that obesity may be associated with a very slight increase in the risk of prostate cancer.

In addition, several studies have found that obese men have a higher risk of aggressive prostate cancer than men of healthy weight. Generally, risk of prostate cancer has been linked to levels of certain hormones and growth factors, especially IGF-1.

Some studies have shown a weak association between increasing BMI and risk of ovarian cancer, especially in premenopausal women, although other studies have not found an association. As with some other cancers, an association between ovarian cancer and obesity may reflect increased levels of estrogens.

Some evidence links obesity to liver cancer and to some types of lymphoma and leukemia, but additional studies are needed to confirm these associations.

Does avoiding weight gain or losing weight decrease the risk of cancer?

The most conclusive way to test whether avoiding weight gain or losing weight will decrease the risk of cancer is through a controlled clinical trial. A number of NIH-funded weight loss trials have demonstrated that people can lose weight and that losing weight reduces their risk of developing chronic diseases, such as diabetes, while improving their risk factors for cardiovascular disease.

However, previous trials and the results of an NCI workshop have demonstrated that it would not be feasible to conduct a weight loss trial of cancer prevention. The reason is that the effect of weight loss on the prevention of other chronic diseases would be demonstrated—and the trial consequently stopped so that the public could be informed of the benefits—before the effect on the prevention of cancer would become evident.

Therefore, most data about whether losing weight or avoiding weight gain prevents cancer come mainly from cohort and case-control studies. Data from these types of studies, called observational studies, can be difficult to interpret because people who lose weight or avoid weight gain may be different in other ways from people who do not, just as obese people may differ from lean people in other ways than BMI. That is, it is possible that these other differences explain their different cancer risk.

Nevertheless, many observational studies have shown that people who have a lower weight gain during adulthood have a lower risk of:

Colon cancer

Breast cancer (after menopause)

Endometrial cancer

A more limited number of observational studies have examined the relationship between weight loss and cancer risk, and a few have found decreased risks of breast cancer and colon cancer among people who have lost weight. However, most of these studies have not been able to evaluate whether the weight loss was intentional or related to underlying health problems.

Stronger evidence comes from studies of patients who have undergone bariatric surgery to lose weight. Obese people who have bariatric surgery appear to have lower rates of obesity-related cancers than obese people who did not have bariatric surgery. It is important to note that whereas most lifestyle weight loss interventions result in weight losses of 7-10 percent of body weight, weight loss from bariatric surgery combined with lifestyle changes generally results in weight loss of 30 percent.

How is NCI studying and supporting research on obesity and cancer risk, and supporting research to understand the populations most at risk?

NCI supports research on obesity and cancer risk through a variety of activities, including large cooperative initiatives, web and data resources, extramural and intramural epidemiologic studies, basic science, and dissemination and implementation resources. The Institute has also issued a number of competitive funding opportunities related to obesity and cancer risk. In addition, NCI is an active participant in the NIH Obesity Research Task Force and played an active role in the development of the 2011 Strategic Plan for NIH Obesity Research. NCI-supported projects are outlined below.

Healthy Nutritional Recipes For Pregnancy

       

Healthy Nutritional Recipes For  Pregnancy

  HEALTHY NUTRITION FOR PREGNANCY

 STEAMED ROHU :-

STEAMED ROHU

A right  food for post natal condition being very healthy and easy to prepare  .A very good source of calcium, protein, and other vitamins & minerals

Ingredients: -
•    Rohu Fish 200gm
•    Mustard seed paste 5gm
•    Poppy seed paste  10gm
•    Cumin seeds 1/2 tsp
•    Garlic cloves 8 to 10
•    Green Chillies  2
•    Coriander  1 tbsp
•    Vinegar 1tsp
•    Oil 1tsp.
•    Banana leaves
•    Lemon wedges 2-3
•    Salt to taste

Preparation: -

1.    Wash the fish.
2.    Sprinkle salt & Vinegar and marinate for 10 minutes.
3.    Grind all the ingredients to form a fine paste for masala.
4.    Spread this paste on the fish and marinate it for 20 minutes.
5.    Spread some oil on banana leaves & wrap each fish in a separate leaf.
6.    Steam the wrapped fillets for 20 to 25 minutes.
7.    Remove from the steamer.
8.    Unwrap and serve hot with lemon wedges.

•      Total quantity: -4
•      Per serving: -2

Nutritive value per serving:

•    Calories(kcal)      109.7  
•    Protein(g)              17    
•    Fat (g)                      2      
•    Carbohydrate(g)    6        
•    Calcium (mg)          729

Green Chapati with Sesame seeds :-


GREEN CHAPATIS

GREEN CHAPATIS

A calcium and beta carotene rich dish which is easy to prepare with easily available food Ingredients This recipe is a good variation of regular chapattis. Inclusion of whole wheat flour would enhance   thiamine and niacin content also

Ingredients:

•    Cauliflower green finely chopped 200gm

•    Sesame Seeds 50gm

•    Bengal Gram Flour 50gm

•    Whole wheat flour 200gm

•    Onion finely chopped 100gm

•    Cumin seeds 5gm

•    Coriander leaves finely chopped 1tsp

•    Cooking Oil 5 ml

•    Red Chili Powder 1/2 tsp

•    Asafoetida 1 pinch

•    Salt to taste

Preparation: -

1.  Dry roast Sesame Seeds.

2.  Mix Bengal gram, whole wheat flour, sesame seeds, red chili powder, turmeric powder, asafoetida,      cumin seeds, coriander leaves and onion in a mixing bowl.

3.  Make dough using some warm water and prepare chapattis.

4.  Serve hot with Yoghurt or Lassi.

        

Total serving: - 15

Nutritive value per serving: - 

5.    Calories (kcal) 89.0

6.    Protein (g) 3.8       

7.    Fat (g) 2.07       

8.    Carbohydrate (g) 13.8   

9.    Fiber (g) 0.73       

10.  Calcium (mg) 146

Note : Ragi flour can be added in proportion of 1:1 with wheat flour as ragi is rich source of calcium.

NUTRITIOUS KEBABS

NUTRITIOUS CHICKEN KEBABS

Tingle your taste buds with enticing and mouth watering Nutritious Kebabs, providing good quality protein and at the same time the goodness of mint and coriander along other ingredients which are loaded with important minerals, vitamins and antioxidants recommended during this stage. Relish these luscious kebabs with green chutney and lemon juice to enhance beta carotene, calcium, vitamin c content among others .



Ingredient

1.    Boneless Skinless Chicken –100 g
2.    Whipping Cream – 5 g
3.    Ginger/Garlic Paste – 1 tbsp
4.    Mint Leaves finely chopped – 1/2 tbsp
5.    Coriander Leaves finely chopped – 1 tbsp
6.    Ground Green Chilies – to taste
7.    Baby Tomatoes-5-6 (for garnishing)
8.    Salt – to taste

Preparation
1.    In a large mixing bowl, mix together all ingredients except chicken. Taste the mixture and adjust
       salt.
2.    Add chicken and mix well.
3.    Cover and keep in the refrigerator to marinate for at least 4-6 hours.
4.    Preheat your oven or grill to a medium high temperature and grill chicken for 8 to 10 min.
5.    Turn the chicken over in between till it turns brown on all sides and is tender.
6.    Garnished with baby tomatoes. Serve hot.

Serves 2

Nutritive value per serving

•    Calories (kcal) 77
•    Protein (g) 12.9
•    Fat (g) 2.8

SOYA SANDWICH


                                     

SOYA SANDWICH

Soya Sandwich, enriched with a filling of soya granules and vegetables, adds spice to nutritious whole wheat bread. An excellent breakfast / evening snack / packed lunch option, rich in good quality protein,  calcium, and dietary fiber making it an excellent snack for lactating women.

Ingredient
•    Soya granules-20 g
•    Brown Bread-4slices (80g)
•    Onion-50 g
•    Tomato-100 g
•    Capsicum-50 g
•    Lettuce leaves (tender) 5 g
•    Black pepper-5 g
•    Oil-10 ml
•    Coriander Leaves5g
•    Red chili flakes-5g
•    Salt
Preparation
1.    Soak Soya granules in warm water for 10 minutes.
2.    Squeeze out all the excess water and keep aside.
3.    Finely chop all the vegetables except lettuce leaves
4.    In a pan heat oil and add all the vegetables, Soya granules, and seasonings.
5.    Sauté well, turn off the flame and keep aside to cool.
6.    Take 2 slices of bread, place a lettuce leaf on one slice, spread the filling on it and cover with the        other slice.
7.    Toast in a non-stick sandwich toaster till crispy golden brown.
8.    Serve hot with chutney /sauce

Serves 4

Nutritive Value per serving
•    Calories (kcal) 130.1
•    Protein (g) 4.5
•    Fat (g) 2.6
•    Carbohydrate (g) 13.7

WHOLE BENGAL GRAM AND CAULIFLOWER KEBABS
                                     

CAULIFLOWER KEBABS

Whole Bengal gram and Cauliflower Kebabs, a variation of the traditional Indian mouth watering snack, made healthy and nutritious to cater for the special requirement of calcium and protein during lactation. It is easy to prepare from readily available ingredients as well as a good alternative to deep fried snacks. Serve with mint- curry leaves’ chutney to enhance beta carotene, vitamin C intake.

.

Ingredient

•    Bengal gram(whole): - 100 g

•    Cauliflower (can use greens also): - 100 g

•    Onions,  100 g

•    Bread crumbs: -50 g

•    Cumin seeds: -1\2 tsp

•    Green Chilies,-3-4

•    Ginger chopped 1tsp

•    Oil 5 ml.

•    Salt to taste 

Preparation

1.    Soak Bengal gram for 3-4 hrs and then grind to a coarse paste by adding enough water.

2.    Grate onion, cauliflower (add shredded greens) & green chilies and mix well to the gram paste.

3.    Add salt, cumin seeds, bread crumbs, ginger. Divide this mixture into equal portions.

4.    Flatten each portion on your palm and shallow fry these kebabs in hot oil.

5.    Once the tikki turn brown in color, remove and serve hot with chutney or sauce.

 Serves 6

Nutritive value per serving

•    Calories (kcal) 107.5

•    Protein (g) 4.8       

•    Fat (g) 2.1       

•    Carbohydrate (g) 17.5   

•    Fiber (g) 1.3

•    Calcium (mg) 147.7

                                        

REFRESHING GRAM DRINK

REFRESHING GRAM DRINK

A nutritious and refreshing beverage adding on the goodness of Bengal gram, ragi flour and yoghurt. A high calcium and protein rich drink made to meet high demands during  lactation.

Ingredient
                                         
•    Roasted Bengal gram flour 100 g
•    Ragi flour 50 g
•    Skimmed yogurt 200 g
•    Ground cumin 5 g
•    Fresh green chili, seeded and very finely chopped-2
•    Fresh finely chopped coriander or mint leaves 10g
•    Salt and pepper to taste
•    Crushed ice
•    Cold water 6 liters.


Preparation
1.    Roast Bengal gram flour and Ragi flour separately.
2.    Pour yoghurt and water in a blender and blend for 1 min.
3.    Add in Bengal gram and Ragi flour.
4.    Add chili, ground cumin, salt and pepper, blend further for 2 min.
5.    Sprinkle cumin powder and coriander/mint.
6.    Serve over crushed ice.
Serves 4

Nutritive value per serving

•    Calories (kcal) 153.4
•    Protein (g) 9.4
•    Fat (g)    1.8
•    Carbohydrate (g) 26.5
•    Calcium (mg) 136.4

CARDAMOM SHAKE

CARDAMOM SHAKE

Cardamom Shake has the added distinct flavor of cardamom and poppy seeds. It is easy to make, delicious, low in fat, good in protein  calcium, and also riboflavin making it an ideal drink for breakfast/ evening tea time.

Ingredient

•    Toned Milk/ Cow’s Milk 300 ml
•    Water 100 ml
•    White Poppy seeds 10 g
•    Cardamom seeds ground 1/2tsp
•    Sugar   10 g( Can be avoided )
   
Preparation

1.    Place the poppy seeds in a frying pan over a moderately low heat and dry-roast, turning often, for        about 5 minutes.
2.    Combine the poppy seeds, cashews or almonds, and water in a blender process for 2-3 minutes.
3.    Add 100 ml of milk and process on low speed for 15 seconds.
4.    Pour the mixture through a strainer over a pan.
5.    Press out as much as liquid as possible, and then add the remaining milk and cardamom seeds.
6.    Stirring constantly bring to boil over moderately high heat.
7.    Reduce the heat to low and simmer for 2 minutes.
8.    Now mix sugar.
9.    Pour the milk back to forth from one pan to another until it is frothy.
10.    Serve immediately in warmed cups.

Serves 2

Nutritive value per serving
•      Calories (kcal) 140.9    
•      Protein (g) 5.88            
•      Fat (g) 7.11  
•     Carbohydrate (g)13.44        
•     Calcium (mg) 259.2    

Guava Drink

GUAVA DRINK

Guava juice is known to be a great thirst quencher as well as an extremely rich source of vitamin C. The flavour of ginger enhances the taste and has many ayurvedic benefits during lactation¬

Ingredients:-
•    Guavas 200 gm
•    Sugar 10 gm( Can be avoided )

•    Juice of 1/2 lemon

•    Ginger juice 1tsp

Preparation:-

1.    Wash and cut the guavas into large cubes.
2.    Place these in a saucepan along with sugar and 1 1/2 cups of water.
3.    Bring to boil and simmer till the guavas are tender.
4.    Cool completely and puree in a blender.
5.    Add ginger and lemon juice and mix well.
6.    Fill half a glass with the pulp and top up with chilled water or ice-cubes and serve immediately.

•    Total serving: - 2

•    Nutritive value per serving: -
•    Calories (kcal) 70.7
•    Protein (g) 0.9    
•    Fat (g) 0.3    
•    Carbohydrate (g) 16.1
•    Fiber (g) 5.2
•    Calcium(mg) 11.5
•    Vitamin C -  212

Soya methi chunks

SOYA METHI CHUNKS

Alongwith the goodness of high quality soya protein, this recipe provides  plenty of Calcium and beta carotene

Ingredients:                                      
•    Soya chunks 50gm
•    Onion 50gm-Chopped
•    Tomatoes 50gm
•    Ginger garlic paste 1/2 tsp
•    Butter 1 tsp
•    Kasoori methi 1 tbsp
•    Turmeric a pinch
•    Red chili powder 1/2 tsp
•    Garam masala 1/2 tsp
•     Milk 50ml
•     Salt

Preparation:-

1.    Wash and pressure cook soya chunks (with water) for one whistle with some salt.
2.     Take out soya chunks, leave them under cold water and squeeze the water out of them.
3.    Heat 1 cup of water and add onion and cook for 5mins, discard water and make a paste.
4.    Blanch tomatoes, peel them and make a paste.
5.    Heat butter in a pan and fry onion paste till golden brown for about 10 min.
6.    Add ginger garlic paste and fry for 2-3 min.
7.    Add tomato paste, mix well and fry for 5 min. Now add all the spices  and cook till the oil leaves the sides.
8.    Add soya to the gravy and add enough water to get a thick consistency.
9.    Add kasoori methi and bring it to a boil.
10.  Remove from heat and add milk and boil it till the gravy becomes thick. Serve hot with chapatis.

•    Total serving: - 2
•    Nutritive value per serving: -
•    Calories (kcal) 164
•    Protein (g) 12.1      
•    Fat (g) 8.4    
•    Carbohydrate (g) 9.9
•    Fiber (g) 1.2
•    Calcium (mg) 113.7

_