By the HPN team.
1. Reduce Sugar
Sugar and other highly processed carbohydrate foods drastically raise blood sugar levels, a situation that is considered very inflammatory and is related to a range of health effects including metabolic disorders, cardiac problems and degenerative brain disorders!
2. Avoid Wheat
Wheat containing products like bread, pasta, cookies and crackers, are some of the primary culprits for the blood sugar related problems mentioned above, but beyond this wheat and one of its constituent proteins gluten may be related to a range of immune problems and direct negative effects in the human brain. While most people don’t have Coeliac disease around 1/3 probably exhibit a type of gluten allergy or intolerance.
3. Eat Good Fats
Fats in general have had a bad rap for many years. The reality is that eating fat does not make us fat, nor does it encourage the adverse cardiovascular effects associated with it. On the contrary fat is important to encourage proper modulation of inflammation and immune status within the body and is associated with providing optimal hormone levels. Eating a higher proportion of natural fats (especially in preference to sugar and highly refined carbohydrates) actually encourages the body to lose fat and maintain a lower level of body-fat.
4. Have Protein at Every Meal
Protein is an essential nutrient. There are several essential amino acids that the body requires in order to create all the various structural proteins that make up the cells, tissues, organs and systems of the body. In fact apart from water we primarily consist of protein structures. Eating sufficient protein not only provides for these requirements but also encourages a greater rate of fat-burning. In fact a higher proportion of protein in the diet has been associated with lower body-fat levels.
5. Eat Six Fist-Sized Servings Veggies!
Vegetables provide essential vitamins and minerals that act like the ‘keys’ that unlock cellular processes. Without these important factors the body is unable to do much of anything! Beyond that though vegetables also provide bulk to the diet and encourage greater feelings of fullness and satisfaction thereby helping us to stay ‘on track’ with our nutrition more often.
6. Eat More Berries
I like to think of berries as ‘nature’s multi-vitamin’. They are nutrient dense, high in antioxidants and relatively low in calories and carbohydrates. Berries have been shown to help reduce oxidative damage that is associated with a range of health and metabolic disorders.
By Cliff Harvey ND
I have back pain. Chronic, annoying, sometimes debilitating back pain. I always figured it was from years of weight lifting and competitive martial arts. But my journey over the years through various diagnoses and treatments had me questioning the solely physical basis for any chronic pain. So what really causes our back pain?
Back pain affects around ¼ of people according to United States national surveys (Deyo, Mirza, & Martin, 2006) but the cause of back pain is still poorly understood. Within a mechanistic model we could make an a priori assumption that the causes are physical dysfunction or injury and this assumption also defines the diagnostic-to-treatment pathway for low back pain which commonly involves referals from a general practitioner to a physiotherapist to a back surgeon or specialist involving various tests along the way.
The challenge within this model of diagnosis and treatment is that there appears to be no firm causal link between the mere presence of spinal pathology (nor its absence) and back pain. A systematic review in Spine concluded that there is indeed no firm evidence for the presence or absence of a causal relationship between radiographic findings (such as disc space narrowing, osteophytes, sclerosis, spondylolysis and spondylolisthesis, spina bifida, transitional vertebrae, spondylosis, and Scheuermann's disease) and nonspecific low back pain (van Tulder, Assendelft, Koes, & Bouter, 1997). Further MRI discovery of bulges or protrusions may be coincidental due to the large amount of people without pain who exhibit the very same spinal anomalies (Jensen et al., 1994). In his 1992 paper in Current Orthopaedic Practice Dr Alf Nachemson states “Rarely are diagnoses scientifically valid, nor is the effectiveness of surgery proven by acceptable clinical trials.” (Nachemson, 1992)
Notwithstanding this intravertebral disk degeneration is a weak predictor of low-back pain in young adults (Salminen, Erkintalo , Laine, & Pentti, 1995), but this statistical correlation does not help the practitioner, nor patient to understand what is actually causing their back pain as there are large numbers of people who exhibit pain with pathology, and large numbers exhibiting pain without pathology.
It is well known that psychological variables (such as pain related to fear) worsen pain (Peters, Vlaeyen, & Weber, 2005). Cohort evidence suggests that low back pain disability is strongly predicted by psychosocial variables and the structural variables (as shown by MRI and discography testing) have only a weak association with back pain episodes and no association with disability or future medical care (Carragee, Alamin, Miller, & Carragee, 2005). A systematic review of prospective cohort studies featuring 20 publications concluded “Psychological factors (notably distress, depressive mood, and somatization) are implicated in the transition to chronic low back pain.” The authors go on to suggest that the development and testing of new clinical diagnostics and interventions taking into account these factors and that there is a need to clarify further the role of psychological factors, especially coping strategies and fear avoidance, in low back pain (Pincus, Burton, Vogel, & Field, 2002).
Serious pathology (such as a fracture) in which we would expect to see resultant back pain is exceedingly rare, accounting for less than 1% of cases of low back pain (Henschke et al., 2009).
Psychosocial factors may be beginning to be further elucidated, at least in a corrolary fashion by neuroimaging evidence suggesting that inappropriate cortical representation of proprioception may falsely signal incongruence between motor intention and movement, resulting in pain in a similar way that incongruence between vestibular and visual sensation may result in motion sickness (Harris, 1999). Others imply that chronic back pain is accompanied by brain atrophy and suggest that the pathophysiology of chronic pain includes thalamocortical processes (Apkarian et al., 2004).
A hypothesis suggested by some is that there is a ‘tension syndrome’ or compartment syndromes (Peck, Nicholls, Beard, & Allen, 1986) present that may help to explain the cause of idiopathic low back pain and that for which we believe (perhaps mistakenly) that there is a physical pathology, and that this may also have a psyco-emotional or psycho-social/psychospiritual basis.
This tension could be related to stress, or a self-limiting belief structure that is attempting to reduce further harm, potential injury or limiting a perceived threat activity, which indeed may or may not be dangerous at all.
There is clinical case series evidence suggesting that this indeed the case and that when people are aware of the reality that back pain may not be a physical dysfunction, but indeed may be simply a stress-tension or psychoneurophysiological inhibition that it may abate. There is scope within this to extend physical therapy into psychological or mind-body therapy modalities if this is indeed the case.
Apkarian, A. V., Sosa, Y., Sonty, S., Levy, R. M., Harden, R. N., Parrish, T. B., & Gitelman, D. R. (2004). Chronic Back Pain Is Associated with Decreased Prefrontal and Thalamic Gray Matter Density. The Journal of Neuroscience, 24(46), 10410-10415. doi: 10.1523/jneurosci.2541-04.2004
Carragee, E. J., Alamin, T. F., Miller, J. L., & Carragee, J. M. (2005). Discographic, MRI and psychosocial determinants of low back pain disability and remission: a prospective study in subjects with benign persistent back pain. The Spine Journal, 5(1), 24-35. doi: http://dx.doi.org/10.1016/j.spinee.2004.05.250
Deyo, R. A., Mirza, S. K., & Martin, B. I. (2006). Back Pain Prevalence and Visit Rates: Estimates From U.S. National Surveys, 2002. Spine, 31(23), 2724-2727 2710.1097/2701.brs.0000244618.0000206877.cd.
Harris, A. J. (1999). Cortical origin of pathological pain. The Lancet, 354(9188), 1464-1466. doi: http://dx.doi.org/10.1016/S0140-6736(99)05003-5
Henschke, N., Maher, C. G., Refshauge, K. M., Herbert, R. D., Cumming, R. G., Bleasel, J., . . . McAuley, J. H. (2009). Prevalence of and screening for serious spinal pathology in patients presenting to primary care settings with acute low back pain. Arthritis & Rheumatism, 60(10), 3072-3080. doi: 10.1002/art.24853
Nachemson, A. L. (1992). Newest Knowledge of Low Back Pain A Critical Look. Clinical Orthopaedics and Related Research, 279, 8-20.
Peck, D., Nicholls, P. J., Beard, C., & Allen, J. R. (1986). Are There Compartment Syndromes in Some Patients with Idiopathic Back Pain? Spine, 11(5), 468-475.
Peters, M. L., Vlaeyen, J. W. S., & Weber, W. E. J. (2005). The joint contribution of physical pathology, pain-related fear and catastrophizing to chronic back pain disability. Pain, 113(1–2), 45-50. doi: http://dx.doi.org/10.1016/j.pain.2004.09.033
Pincus, T., Burton, A. K., Vogel, S., & Field, A. P. (2002). A Systematic Review of Psychological Factors as Predictors of Chronicity/Disability in Prospective Cohorts of Low Back Pain. Spine, 27(5), E109-E120.
Salminen, J. J., Erkintalo , M., Laine, M., & Pentti, J. (1995). Low Back Pain in the Young A Prospective Three-Year Follow-up Study of Subjects With and Without Low Back Pain. Spine, 20(19), 2101-2107.
van Tulder, M. W., Assendelft, W. J., Koes, B. W., & Bouter, L. M. (1997). Spinal radiographic findings and nonspecific low back pain. A systematic review of observational studies. Spine (Phila Pa 1976), 22(4), 427-434.
By Cliff Harvey ND
“Cliff – I read that Alfalfa might be linked to Lupus? That sounds incredible! Is it true?”
There may be some truth to this statement. While it seems incredible that a common food such as Alfalfa may be linked to triggering Lupus (Systemic Lupus Erythmotosus – SLE) there is evidence that alfalfa triggers an SLE like illness in monkeys (Bardana Jr et al., 1982; Malinow, Bardana, Pirofsky, Craig, & McLaughlin, 1982).
Lupus is an autoimmune condition is a systemic autoimmune disease that can affect any part of the body. In autoimmune diseases the immune system attacks the body's cells and tissue, resulting in tissue damage and excessive inflammation.
There is an amino acid present in alfalfa called L-canavanine, not required by the human body to create proteins but which triggers immune effects in primates and it is thought that L-canavanine directly affects immune function in humans (Alcocer-varela, Iglesias, Llorente, & Alarcón-Segovia, 1985).
It is now commonly recommended that people with autoimmune conditions and lupus in particular avoid alfalfa (Patavino & Brady, 2001).
Alcocer-varela, J., Iglesias, A., Llorente, L., & Alarcón-Segovia, D. (1985). Effects of L-canavanine on t cells may explain the induction of systemic lupus erythematosus by alfalfa. Arthritis & Rheumatism, 28(1), 52-57. doi: 10.1002/art.1780280109
Bardana Jr, E. J., Malinow, M. R., Houghton, D. C., McNulty, W. P., Wuepper, K. D., Parker, F., & Pirofsky, B. (1982). Diet-Induced Systemic Lupus Erythematosus (SLE) in Primates. American Journal of Kidney Diseases, 1(6), 345-352. doi: http://dx.doi.org/10.1016/S0272-6386(82)80005-X
Malinow, M., Bardana, E., Pirofsky, B., Craig, S., & McLaughlin, P. (1982). Systemic lupus erythematosus-like syndrome in monkeys fed alfalfa sprouts: role of a nonprotein amino acid. Science, 216(4544), 415-417. doi: 10.1126/science.7071589
Patavino, T., & Brady, D. M. (2001). Natural medicine and nutritional therapy as an alternative treatment in systemic lupus erythematosus. Alternative medicine review : a journal of clinical therapeutic, 6(5), 460-471.