Written by: Dr. Brandon Brock, MSN, BSN, RN, NP-C, DCN, DCM, DAAIM, BCIM, DACNB, FICC (Head Clinician Cerebrum Health Centers)
Structural content edited by: Tara Brock
Your “Sugar Daddy” might actually be Messed up in the Head
I live in Texas, and for some reason, this is the blood sugar dysregulation capital of the world – likely diet. It is very clear as to how blood sugar problems impact the brain, but not a lot of clinicians make the connections. You really cannot do anything to the brain, if Insulin and blood sugar are off from a clinical perspective, and hopefully and will show you that. The fuel for delivery will not allow adequate cellular energy mechanics to work properly and they will fatigue and people will fade as the day goes on or if therapy is to robust. So we know that having bad or fluctuating sugar changes brain, but what does a bad brain do to blood sugar? Can having bad neurological based cellular or specific brain region dysfunction actually in return alter blood sugar readings, insulin function and stability as it pertains to the glycemic story? That is what we are going to explore today.
If a person has unhealthy neurons or brain cells, this can cause a problem. For instance, if there is
inflammation, alcohol abuse, bad diet, bad genetic make up, infection,stress, radiation, trauma, low blood flow, autoimmunity and so on, then you can get neuronal stress. The metabolic demands and needs of a neuron require glucose, especially if injured. If there are multiple cell bodies that are injured, this could create hypoglycemic moments, especially when the person is trying to utilize their brain, at a high capacity because damaged neurons suck up more glucose, leaving less in the blood. Hello hypoglycemia. This can create multiple blood sugar symptoms: including tremors, mood changes, behavioral fluctuations, and many other neurological problems, depending on what the underlying terrain and function of the brain is without having low blood sugar. Hypoglycemia without a known cause can warrant the need to look at the brain, especially if the person experiences neurological changes when it drops or if using the brain excessively makes it worse.
The take home message
- Know if you have hypoglycemia (If so – preferably why).
- Know if the hypoglycemia presents with brain changes (If so – where).
- Know if fatiguing the brain makes blood sugar drop (If so – how much and how fast).
- Determine if there is a change in the left or the right hemisphere (If so which side).
- Determine if the entire brain is suppressed along with cognitive function that has failed (If so, are there any co-morbidities perpetuating inflammation).
- Correlate the brain and blood sugar reading to determine if you have cellular dysfunction and energy kinetic issues. This could be an early sign of neurodegeneration and needs to be corrected
Next, if you have a decrease in overall cerebral function, there can be some real issues. For
instance, with head trauma, inflammation in the brain and so forth not only increase the cellular demand as just mentioned, it can also alter the function to the hypothalamus and then ultimately to the pituitary. The alteration in this hypothalamic – pituitary axis can seriously create a situation of insulin resistance and hypoglycemia susceptibility. For example, with a head injury, we also compare blood sugar and A1c and we always look at total and free insulin and Cpeptide. We have statistical correlation maps made for these values to determine if insulin and glucose are doing the same thing and if there is a Type II presentation or type I presentation of pathology, how bad it is or, is there a combination of both presiding. So if the person has individual cell damage and then on top of that, hemisphere shifting, it could alter blood sugar stability greatly.
Take home message
- Know if you have blood sugar problems. (Again, now why).
- Know if fatiguing the brain makes blood sugar drop (This is a HUGE clinical nugget)
- Determine if there is a change in the left or the right hemisphere (Work by stressing each).
- Determine if the entire brain is suppressed along with cognitive function that has failed (Observe).
- Determine where the area of dysfunction is and then determine the cause and other comorbidities that might be behind the problem (Start to build the story).
The Cerebellum gives us the gift of smooth and coordinated movement and even goes to the midbrain and contralateral brain and the brainstem for control, drive, modulation and mechanistic integration into high complexity movement and function. The cerebellum fires to the mesencephalon and various vital centers, which can increase the need for glucose demand. This is especially true when it comes to the IML and the sympathetic chain being abnormal, which can lead to an abnormal drive of epinephrine and norepinephrine that drives the tissues needs for glucose and can cause blood sugar to drop. The deep cerebellar nuclei are typically stimulating in nature and there is a surround inhibitory mechanism that is driven by the purkinje system. When this goes, then we typically see escape mechanisms and this can in return cause or create summation in the pons and in the mesencephalon and create a real issue with over activation or erratic control of the autonomic nervous system, which will burn and utilize fuel differently. This can even impact the vestibular system. If the patient has coordination issues, a loss in smooth movement, intention issues and various types of tremor, then this area needs to be considered as a culprit if there is blood sugar, insulin or dysglycemic presentation. It is tough to say which came first, the cerebellar or the Blood sugar issue, but rest assured that if there is a cerebellar physiological shift and the patient has blood sugar or dysglycemic tendencies, then they will develop problems and one thing that will happen is that they will perpetuate each other and healing will not begin until both change. A good clinical example would be dietary changes for the blood sugar, dietary changes that help cerebellar antibodies, activation of the cerebellum that is appropriate and then working to get all components of physiology and neurological functional neurology to work together.
Take Home Message
- Is there a blood sugar problem that is not part of a bad diet or genetic issues?
- Is there a blood sugar problem with poor coordination or essential or intention breakdown?
- Are there cerebellar antibodies present in the patient or Gad antibodies?
- Is the patient on GABAergic meds or have they been or quit (Benzos)?
- Does the person drink excessively or have a severe B deficiency?
- Does the patient has gait changes or ataxia or changes in speech coordination or loss in smooth ocular pursuits or end gaze nystagmus or vertical nystagmus along with any of the aforementioned.
- Does the patient have a foot deformity with high arches and hammer toes?
The basal ganglia are a delicate balance of the brain being able to activate or inhibit various subcortical circuits that make the brain go or stop. Many neurotransmitters are used to do this and that includes ACH, dopamine, glutamate and GABA. Basal ganglionic lesions create a lot of problems with tremor, speed and slowness or capacity to have movement and a lot of times, there are hyper or hypokinetic disorders. Hyper kinetic disorders are situations where the brain is in overdrive due to the direct pathway doing into over time. We see this when dopamine from the ventral tegmentum hits the neostriatim and primes D1 receptors and facilitates activation. This sometimes makes exaggerated motor, emotional or perceptual responses. On the flip side, there is the indirect pathway that at times can really stop all activation and make people hypokinetic if dominant. The direct pathway and the indirect pathway need to be understood and then the movement disorders and the projections from there can be further understood.
If someone tilts to the direct pathway for dominance, either as a result of injury plastic changes, meds or autoimmunity, then the body will go into over drive. This has a tendency to create more need for blood sugar and can cause exhaustion to supplies and amounts and drive people into glycemic problems. Some people with persistent autoimmunereactions to the basal ganglia as a result of strep cross reactivity end up getting significant taxing of the direct pathway going full speed at all times and the patient cannot slow down or sit still or control moods or control emotions. This becomes a really bad problem for the patients and the patient because much of it is reflexogenic and not learned behavior.At times T regulatory systems, underlying infections agents, biofilms, immune polarization and any underlying co-morbidities have to be dealt with in some of these autoimmune issues that will create a PANS type of situation.
One thing that all may have in common is that when the immune issue drives the direct pathway, the blood sugar can drop and this can perpetuate poor behavior. At some point being able to look at the patient and determine if the basal ganglia is damaged in a patient from a clinical perspective is very important. Learning about movement disorders and what they do to blood sugar, blood sugar regulatory systems and other autonomic and adrenal responses is very important to understand.
Take Home Message
- Is there a blood sugar disorder that has signs and symptoms of basal ganglia disease?
- Is the patient on GABA, dopamine or ACH altering meds. They can all impact the basal ganglia?
- Does the patient have any physical or mental hypo or hyper kinetic conditions?
- Is there hand writing problems, anxiety, insomnia or a loss in cortical control mechanisms?
- Is there a history of repeated infectious disease or head injury?
- Is there a family history of problems for the patient?
- Is there rigidity, a resting tremor, a mask face, problems ambulating and so forth.
Medial Temporal Lobe
With a decrease in medial temporal lobe function many things can happen clinically. One thing that is very significant is that it changes the function of the hippocampus. When the hippocampus region is changed, one thing that happens over times is short term memory loss, but earlier than that is the development of circadian rhythm changes, blood sugar fluctuations and depression. The depression typically happens before the memory loss. I always clinically look for depression, an alter ASI curve and blood sugar fluctuations at the same time and then I ask if there are any mild slips in memory. When I see these things it cues me to work on these regions from a plasticity point of view. Over time, if there is neuro-degeneration, excito-toxicity, accumulation or tau proteins, vascular disease or insult or excessive cortisol, then the temporal lobes and the hippocampus are going to get blasted. The visual-spatial loss that happens as a result along with Impaired declarative memory can really suggest progression of the condition. Having an inability to remember facts and autobiographical events is a very bad sign. When cortisol is off blood sugar will be off and the patient will have issue with getting up, staying awake in the afternoon, problems with sleeping and problems with staying asleep when falling asleep. There are problems with fluctuations in insulin resistance and hypoglycemia. These are important because they could be early signs of progressive dementia, despite the type that it may be. Neurologically there can be various behavioral changes that occur, that get exacerbated during hypoglycemia and various forms of ocular pursuits will be altered as well.
Take Home Message
- Are there blood sugar fluctuations?
- Are there findings of depression?
- Is there a progressive loss of memory?
- Are there problems getting up, staying up or sleeping?
- Is there a loss of visual – spatial memory?
- Is there excito-toxicity noted in the patient, is the patient intolerant to MSG or artificial sweetner’s?
- Is the patient taking medications that modulate ACH?
- Is the patient taking meds that modulate NMDA receptors like Namenda?
This is an area that is greatly overlooked in the world of blood sugar variability. Anytime there is autoimmunity, obesity or underlying infection or other conditions like thyroid pathology, the immune system has a chance to go haywire. One thing that is noted is that a patient can have Islet cell, insulin or Gad-65 antibodies, all of which can lower the ability to produce insulin. This can be noted on antibody testing and seen in real time with glucose tolerance tests that go for about three hours. You can watch insulin fail, or if you measure C-peptide, it will start to drop or fluctuate. With patients that have anxiety, blood sugar fluctuations and insulin changes, there is a large capacity for GAD – 65 antibodies to be present. GAB also turns glutamate into GABA and if the patient has autoimmunity to that, then the patient can develop glutamate build up with not enough GABA to compensate and the patient gets anxious.
As a result, the cerebellum can be impacted, the basal ganglia can be impacted, insulin can be abnormal, the immune system can be dysregulated, a patient can get chemically intolerant and many conditions can start to develop. Inflammation itself, that happens as a result of any cause, can do many things pathologically. This can be responsible for more insulin resistance, leaky gut, more cytokine release, immune dysregulation, autoimmunity, chemical sensitivities, cancer or hepatic biotransformation issues. The bottom line is, you do not want to be chronically inflamed and you do not want to be so messed up with the immune system that it created autoimmunity. The interesting thing, is that all the conditions that are created by inflammation, end up creating more inflammation. This is the loop that can spiral out of control and really cause a lot of problems. If insulin becomes low, there are a lot of problems that can develop as a result. The patient can lose brain derived neurotropic factors and cellular stability can be hurt.
Take home message
- Is the patient having have blood sugar regulation issues?
- Does the patient have elevated thirst, hunger or urination?
- Is the patient losing weight, muscle tissue or strength?
- Is there a GTT, c peptide or blood glucose abnormality?
- Is there anxiety, insomnia or emotional disorders?
- Is there a lot of “end organs” involved and does the patient have a lot of pathology on Cyrex panel 5?
- Is there multiple chemical sensitivities, liver issues, a leaky gut or multiple areas of inflammation?
- Does the brain globally have problems due to insulin and or dysglycemia along with autoimmune disease?
We could go all day about what diet means as it pertains to glucose, calories, protein and how the body processes energy. At times caloric restrictions can help with healing and help with autophagy. Many times fasting will help a patient has a much lower antigen load. I would also say that not all ketogenic diets or paleo situations work. Some patients will go on a diet with very healthy and “clean” foods and the patient is actually eating carbs that feeds their SIBO, or makes overgrowth in the guts worse which promotes inflammation and then you get all the things this paper has to offer. I would also add that many patient’s cannot tolerate various foods and if there is no clinical monitoring or testing, the patient may be eating foods that makes the patient have inflammation, abnormal blood sugar utilization and many other things can occur.
So diet can control the nutrients, the calories, the ability to heal, the ability to reduce an antigenic load and help reduce SIBO, histamines, oxalates, and other food reactions. Diet has everything to do with making a patient have good bloodsugar, less inflammation and help control a number is diseases or issues that a person might have.
Take home message
- Do you have food reactions?
- Do you have bloating after eating?
- Have you had a head injury?
- Do you have problems with blood sugar control?
- Do you have problems with histamines?
- Do have kidney or oxalate issues?
- Do you have a high antigen load?
- Are you irritable before meals or do you get tired after eating?
Exercise and receptor base activation
Exercises burns blood sugar and this can be, unless you have type 1 diabetes and the patient cannot utilize enough sugar to perform, then you have major health issues to deal with. Overall, exercise is still the best. It helps with a number of different metabolic processes and the patient can easily do a lot with blood sugar control, opiate levels, BDNF, growth hormone and more. Exercise, including burst and interval training and high intensity has the greatest impact on all issues that are really good for brain. The aforementioned are a bid deal, but nitric oxides are a really big factor impacted by exercise, which can help with blood flow and cell healing. Insulin receptor sensitivity is improved and the patient will have less oxidative stress and will also have immune enhancement. Multiple medications can impact blood sugar and lipids, many of these patients including those of the psychotropic realm. Receptor based stimulation also does a lot for the brain as demonstrated below.
Take home message
- Does your patient exercise?
- Is there an issue with insulin resistance, weight gain or a pear shape including belly fat?
- Does the patient have a lot of pain?
- Does the patient need immune enhancement or and immune regulation?
- Is there blood sugar control issues that are part of a sedentary lifestyle?
The aforementioned figure is a synopsis that represents the entire story of the paper that is being presented today.
References and Citations
Thank you to Datis Kharrazian donations of information.
- G. Bazzu, G. G. Puggioni, S. Dedola, G. Calia, G. Rocchitta, R. Migheli, M. S. Desole, J. P. Lowry, R. D. O’Neill, P. A. Serra, 2009 Real-time monitoring of brain tissue oxygen using a miniaturized biotelemetric device implanted in freely-moving rats. Anal. Chem., 81 2235 2241.
- G. Calia, G. Rocchitta, R. Migheli, G. G. Puggioni, Y. Spissu, G. Bazzu, V. Mazzarello, J. P. Lowry, R. D. O’Neill, M. S. Desole, P. A. Serra, 2009 Biotelemetric Monitoring of Brain Neurochemistry in Conscious Rats Using Microsensors and Biosensors. Sensors, 9 2511 2523 .
- M. A. Castro, F. A. Beltrán, S. Brauchi, I. I. Concha, 2009 A metabolic switch in brain: glucose and lactate metabolism modulation by ascorbic acid. J Neurochem.,110(2),423-440.
- J. Emerit, M. Edeas, 2005 Neurodegenerative diseases and oxidative stress. Eur. Neuropsychopharmacol., 15 100 101 .
- M. Fillenz, J. P. Lowry, M. G. Boutelle, A. E. Fray, 1999 The role of astrocytes and noradrenaline in neuronal glucose metabolism. Acta Physiol. Scand., 167 275 284 .
- M. Fillenz, 2005 The role of lactate in brain metabolism. Neurochem. Int., 47 413 417 .
- J. P. Lowry, M. Miele, R. D. O’Neill, M. G. Boutelle, M. Fillenz, 1998 An amperometric glucose oxidase/poly(o-phenylenediamine) biosensor for monitoring brain extracellular glucose: In vivo characterisation in the striatum striatum of freely-moving rats. J. Neurosci. Methods, 79 65 74 .
- O. M. Schuvailo, O. Soldatkin, O., A. Lefebvre, R. Cespuglio, A. P. Soldatkin, 2006 Highly selective microbiosensors for in vivo measurement of glucose, lactate and glutamate. Analytica Chimica Acta, 573 110 116
- Y. Watanabe, B. B. Hyllbrant, B. Langstrom, 1997 Tracing oxygen metabolism by use of positron emitter Oxygen-15. Biochem. Biophys. Res. Commun., 231 131 134 .
- R. Wilson, A. P. F. Turner, 1992 Glucose oxidase: an ideal enzyme. Biosens. Bioelectron., 7 165 185. Capuron, L. (2011). Pharmacology & Therapeutics. Pharmacology & Therapeutics, 130, 226–238.
- http://doi.org/10.1016/j.pharmthera.2011.01.014Maalouf, M., Rhob, J., & Mattson, M. (2009). The neuroprotective properties of calorie restriction, the ketogenic diet, and ketone bodies. Brain Research Review, 59, 2 9 3 – 3 1 5.
- http://doi.org/10.1016/j.brainresrev.2008.09.002Miller, A., Maletic, V., & Raison, C. (2009). Inflammation and Its Discontents: The Role of Cytokines in the Pathophysiology of Major Depression. BIOL PSYCHIATRY, 65, 732–741. http://doi.org/10.1016/j.biopsych.2008.11.029