Vascular dementia is a condition caused by a blockage preventing blood flow or reduced blood flow to the brain. Once brain cells are deprived of oxygen and nutrients carried by the blood, they die. Brain cell death causes dementia.
Recent research goes further and is recommending a “life-course” shift to maximize your ‘windows of opportunity,” in preventing vascular dementia.
Doctors are stressing that mid-life patients:
Manage Hypertension: Studies suggest increased dementia risk for people with hypertension.Researchers in the United Kingdom suggested that “Increased Blood Pressure) variability is associated with poorer cognitive function in older people and may represent a novel modifiable risk factor for cognitive decline.(1)
Manage their Diabetes: Researchers in Spain suggest that “It is important for physicians responsible for the metabolic control of diabetic patients to know this possible association (Between diabetes, dementia, and Alzheimer’s disease) and to explore cognition in the control visits of patients with Diabetes.”(2)
Explore hormone replacement therapy and treat depression.
Research in the journal Current opinion in psychiatry, (3) suggests
Other evidence suggests that:
insomnia, cognitive stimulation and social activities, head injury, diet, and and oral health should be explored in making a plan for Vascular dementia risk reduction.
The connection between vascular disease and dementia has been well documented by science and the connection between the two is something we explore in our patients.
Research highlights from a study from the Indiana University School of Medicine (4) suggest:
Young-onset dementia is a neurologic syndrome that affects behavior and cognition of patients younger than 65 years of age. Although frequently misdiagnosed, a systematic approach, reliant upon attainment of a detailed medical history, neuropsychological testing, laboratory studies, and neuroimaging, may facilitate earlier and more accurate diagnosis with subsequent intervention.
The differential diagnosis of young-onset dementia is extensive and includes early-onset forms of adult neurodegenerative conditions including:
- Alzheimer’s disease, vascular dementia,
- Frontotemporal dementia, (this is an umbrella term to describe problems of the generally associated with the frontal and temporal lobes of the brain. These are the areas that impact personality, behavior and language.)
- Lewy body dementias, (abnormal protein deposits in the brain that affect thinking, movement, behavior, and mood.)
- Huntington’s disease, (A progressive and fatal breakdown of nerve cells).
- and Prion disease. (Brain damaged caused by abnormal prion proteins in cells).
Late-onset forms of childhood neurodegenerative conditions may also present as young-onset dementia.
Potentially reversible etiologies including inflammatory disorders, infectious diseases, toxic/metabolic abnormalities, transient epileptic amnesia, obstructive sleep apnea, and normal pressure hydrocephalus (intracranial pressure) also represent important differential diagnostic considerations in young-onset dementia.
Cardiovascular and Vascular dementia treatment
In the journal Seminars in Neurology, (5) researchers wrote: “Cardiovascular disease and dementia are common in the elderly and are major causes of disability in the general population. Epidemiological studies suggest that these once believed unrelated conditions, heart disease and dementia, may be linked by shared common risks and pathogenic elements.
These observations have sparked the notion that prevention or modification of certain vascular risk factors and proper management of cardiovascular disease may prevent the development or progression of dementia including Alzheimer’s disease.”
Research from the University of Illinois College of Medicine at Chicago suggests (6): “Vascular disease is associated with increased risk of dementia. Vascular health worsens with age….The findings (of this study) support the view that cerebral small vessel disease and cardiovascular disease are inter-related…the findings add weight to the argument for strategies to improve general cardiovascular health as a potential preventative strategy against cognitive decline in later life.”
In research at the British Medical Journal, (7) University College London health care professionals followed more than 7,000 men and women ages 45 to 70 over a 10-year period to rate their brain decline as they aged.
The study showed that men aged 65-70, there was a 9.6% decline in mental reasoning while women suffered a decline of 7.4%. However, what they found most alarming was in both men and women between the ages of 45-49 showed a 3.6% decrease in brain function.
This is what the researchers said “Adverse cognitive outcomes like dementia are now thought to be the result of long term processes over at least 20-30 years leading some authors to argue for the importance of approaches during life.
Despite much research on early diagnosis, pathophysiological and clinical studies have yet to identify biomarkers or cognitive profiles that accurately predict dementia.
Nevertheless, there is enough evidence to show the importance of healthy lifestyles and cardiovascular risk factors in adulthood for dementia.
For some of these risk factors, such as obesity, hypertension, and hypercholesterolaemia, it is mid-life levels that seem to be more important than those measured at older ages.
There is emerging consensus that “what is good for our hearts is also good for our heads,” making aggressive control of behavioural and cardiovascular risk factors as early as possible key targets for clinical practice and public health.”
What the British researchers are stressing is not that brain decline occurs, but the surprise at the rate of decline that begins in the mid 40’s and the lifestyle and dietary lifestyles that need to be addressed to help patients have both a health heart and mind.
Managing and treating vascular disease risk factors are not only beneficial to preventing heart disease and stroke, but also common forms of dementia.
At the Magaziner Center for Wellness, we approach dementia by creating an individualized, patient-centered treatment plan.
Every person has a unique biochemistry which reacts to pollutants and toxins differently. In order to determine the factors that underlie each case, we utilize extremely thorough blood and urine tests, as well as a complete examination of every aspect of the body, from mitochondrial function to nutrient imbalances to heavy metal toxicity. We recommend dietary modifications to reduce foods that may cause inflammation while increasing intake of those that are anti-inflammatory. Brain inflammation has been a hallmark of dementia and memory decline.
The treatment plan based on these findings may include chelation therapy, hyperbaric oxygen therapy, antioxidant nutritional supplements, intravenous vitamins, regenerative therapies, diet and nutrition.
If you would like to explore more information, please contact our office so we can start a conversation with you.
1 McDonald C, Pearce M, Kerr SR, Newton JL. Blood pressure variability and cognitive decline in older people: a 5-year longitudinal study. J Hypertens. 2017 Jan;35(1):140-147.
2 [Dementia and diabetes: Casual or causal relationship?] Med Clin (Barc). 2014 Mar 12. pii: S0025-7753(14)00119-5. doi: 10.1016/j.medcli.2014.01.026. [Epub ahead of print]
3 Rooney RF. Preventing dementia: how lifestyle in midlife affects risk. Curr Opin Psychiatry. 2014 Jan 16. [Epub ahead of print]
4. Kuruppu DK, Matthews BR. Young-onset dementia. Semin Neurol. 2013 Sep;33(4):365-85. doi: 10.1055/s-0033-1359320. Epub 2013 Nov 14.
5. Muqtadar H, Testai FD, Gorelick PB. The Dementia of Cardiac Disease. Curr Cardiol Rep. 2012 Sep 12.
6. Richardson K, Stephan BC, Ince PG, Brayne C, Matthews FE, Esiri MM. The Neuropathology of Vascular Disease in the Medical Research Council Cognitive Function and Ageing Study (MRC CFAS). Curr Alzheimer Res. 2012 Apr 2.
7 Singh-Manoux A, Kivimaki M, Glymour MM et al. Timing of onset of cognitive decline: results from Whitehall II prospective cohort study. BMJ 2012; 344 doi: 10.1136/bmj.d7622 (Published 5 January 2012)