You may have heard that weight gain is not good for you but did you know that those extra pounds of fat may literally make you grow old before your time? We are not talking about the normal signs of aging like wrinkles or gray hair. Instead researchers have been uncovering what happens deep down at cellular level when cells show telltale signs of accelerated aging when weight is gained or resistance to the hormone insulin is present.

Most of us never give our blood glucose levels a second thought and it used to be that only diabetics had to worry about it but not so anymore. All of us are now becoming more susceptible to a nasty disease that is becoming more prevalent around the world.

This most common and overlooked modern chronic lifestyle disease is caused by your body’s ability to process the food you eat and you may already be suffering from it. Although insulin resistance has been known about for decades, it is only in the last ten years how it derails your health is being better understood.

As many as one in four of us is in this pre-diabetic state without even knowing it and one in three of us will actually go on to develop full blown diabetes. This condition could easily knock 15-20 years off your lifespan so it is a serious health issue.

Our busy modern day lifestyles can cause us to neglect the very basics of self care – proper nutrition and proper exercise. Both of these things are pushed to the back burner when we are pushed for time yet both of them should be at the top of your ‘to do’ list. Diabetes is 80 percent preventable and these two things are what are needed to prevent it.

The human body functions best when blood sugar levels are balanced yet we over-consume highly refined carbohydrates like bread, pasta, sugary foods and drinks and our body simply gets overwhelmed and cannot clear the sugar from the bloodstream. High insulin levels along with high blood sugar levels cause damage to every tissue and organ they touch when they circulate around the body with nowhere to go.

The negative consequences of high blood sugar can take years to become apparent but make no mistake if you are eating a low quality (mainly processed) diet and live a no exercise lifestyle the damage is happening inside you and cannot be repaired.

You can easily do a self assessment as you may be experiencing some or all of the classic symptoms such as weight gain (especially round the midsection) feeling tired and listless and lacking motivation to exercise or be active. Your blood pressure may be creeping upwards and food cravings from unbalanced hormones may be forcing you to eat more than you should.

If this sounds like you it is time to take a detour so you do not end up with the silent killer diabetes. Although it is called a killer you do not die from it, you die from the damage it does to important organs that you need to stay alive. This makes it so deadly because you do not feel anything wrong so do not underestimate what is happening inside.

Those two simple strategies – firstly, a proper strength training program performed 2-3 times each week will help use up excess sugar from the blood stream as the muscle cells are where fuel (food) is burnt for energy so get them strong and toned. Next ditch the processed food and replace it with natural whole foods cooked from scratch at least 80 percent of the time.

Within weeks of implementing these two things you will feel much better and will have more energy so exercising becomes more enjoyable. It is far easier to hang on to the good health you have right now than wait till the wheels fall off and your health is lost. Do not wait till this disease hunts you down and picks you off, be proactive and make sure it will never make you a victim.

A neuropathic ulcer was defined as a full-thickness skin defect produced, in the absence of ischemia, as the consequence of loss of protective sensation or of a deformity due to a motor neuropathy, sometimes aggravated by autonomic alterations. Callus is observed covering the lesion or at its margins, and these ulcers usually bleed easily. Neuropathic ulcers often appear at points of sustained low pressure or shear over a bony prominence.

A neuroischemic ulcer is a full-thickness skin wound whose underlying cause is both peripheral neuropathy and peripheral arterial disease. Despite ischemia, symptoms may be absent. The wound base is ulcerous, sphacelated, or necrotic. Bleeding is absent or only slight. Neuroischemic ulcers often appear in the dorsal and lateral zones of the foot as the consequence of a small traumatic injury or shear.

Neuropathy was diagnosed by examining 10 sites on the foot using a Semmes-Weinstein monofilament 5.07 10 g (Sensifil-Novalab Ibérica, Madrid, Spain) and a Horwell 997 neurotensiometer (Sensifil-Novalab Ibérica). Vascular involvement was defined as an ankle-arm index <0.8, transcutaneous oxygen tension (TcPo2) (using a TCM4 transcutaneous monitor; Radiometer Medical, Brønshøj, Denmark) <30 mmHg, and lack of a dorsal pedal and posterior tibial pulse. Wound infection was clinically defined according to the criteria of the International Working Group on the Diabetic Foot (IWGDF) as the presence of two or more signs and symptoms of local inflammation or systemic signs of infection of no other apparent cause, along with a purulent exudate. In addition, we also looked for specific signs such as necrosis, delayed wound healing, foul odor, and bone exposure. Soft tissue specimens for culture were obtained after brief cleaning of the ulcer surface with saline and sterile gauze. Samples of exudate were obtained by rubbing the surface with a sterile cotton swab, and deep tissue samples were obtained using a no. 10 or 15 scalpel blade (CE 0086; Swann-Morton, Sheffield, U.K.). Specimens were transferred to a sterile vessel containing transport medium (CE 0344; Copan Innovation, Brescia, Italy) and submitted to the microbiology laboratory for culture. We assessed the ulcers according to the classification schemes of Wagner and Texas to record the extension and depth of all soft tissue lesions and detect any evidence of bone infection. In addition, a PTB test was performed in all patients using a blunt, sterile, metal surgical instrument to gently explore the ulcer. The test result was scored positive when a hard substance assumed to be bone was palpated accompanied or not by deep sinus tracts. The PTB was always conducted by the same experienced podiatrist.

In Spain, amputations due to osteomyelitis are performed each year in 46.1 of every 100,000 individuals with diabetes. In diabetic patients, approximately two-thirds of all amputations are preceded by the infection of a foot ulcer. However, the diagnosis of chronic osteomyelitis in the diabetic foot continues to be a challenge, and we believe that there is a need for more studies validating the different diagnostic methods available. There is also a clear need for a safe, rapid, and efficient diagnostic protocol designed to optimize the therapeutic approach and improve the prognosis in these patients.

The early suspicion of osteomyelitis is essentially clinical and is based on detection of the presence of signs and symptoms of infection, although many patients have no typical local signs. Even in the absence of clinical signs, most infected chronic ulcers of the diabetic foot have underlying osteomyelitis. A lack of clinical signs can lead to a delay in diagnosing the initial stages of infection.

The plain X-ray is not useful for detecting bone infection in the first 2 weeks. Bone abnormalities can generally not be seen until bone mineral density drops to 35–50% of that of normal adjacent bone. Moreover, subtle changes at the onset of osteomyelitis are not easily distinguished from other changes that occur in the feet of these patients due to their neuropathy or peripheral vascular disease.

The probe-to-bone (PTB) test is routinely performed to detect, using a blunt instrument, palpable bone through the ulcer, indicating osteomyelitis. However, this test has been validated only in a few previous studies, and there is currently no consensus on a standardized protocol for the clinical diagnosis of osteomyelitis. The present study provides data on the validity of the clinical tests most frequently used to detect this disease.

This observational, descriptive study with prospective collection of data was conducted in patients with type 1 or 2 diabetes who attended the Diabetic Foot Clinic of the University Podology Clinic, Universidad Complutense de Madrid (Spain) because of a foot ulcer.

Over the period May 2006 to November 2008, we treated 210 foot lesions in diabetic patients. Of these lesions, 132 with clinical suspicion of infection were selected as the study sample, of which 105 (79.5%) were finally diagnosed as osteomyelitis. Infection was recorded according to the presence of clinical signs and symptoms and a positive soft tissue culture result. Once infection of the ulcer had been established, presumptive osteomyelitis was diagnosed by plain radiography and a clinical examination.

Patients were enrolled if they had a single ulcer of neuropathic or neuroischemic etiology below the ankle, there was suspicion of bone infection according to clinical signs and symptoms and the diagnostic tests standardized in the protocol used at our center (ulcer specimen culture, radiography, and PTB), if they had undergone surgery for acute osteomyelitis, or if after adequate local or antibiotic treatment and rest, the ulcer did not resolve. Patients were excluded if they had critical ischemia according to the classification of Fontaine et al. or were due for an operation that was unrelated to a diagnosis of osteomyelitis. The study protocol was approved by our institutional review board.